Cerebellar involvement in Parkinson’s disease resting tremor

Lefaivre, Shannon C.; Brown, Matt J. N.; Almeida, Quincy J.

doi:10.1186/s40673-016-0051-5

Cited by 18 publications

(15 citation statements)

References 24 publications

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“…An important aspect that one has to bear in mind when interpreting patterns of activity in M1 is the fact that M1 is the target of somatotopically organized outputs from both the basal ganglia and cerebellum . Although it is not clearly understood how the basal ganglia and cerebellum interact with each other, there is increasing evidence on the involvement of the cerebellum in resting tremor in PD, and it could be that information processing along this parallel pathway connecting the cerebellum to cortical motor areas contributes to and modulates the pathophysiological state of M1 in PD. Finally, although the existing dichotomy of functional activity in M1 as revealed by nuclear imaging and MRI may seem somewhat contradictory, it also raises the question whether PD may be associated with a patterned combination of hypo‐ and hyperactivity.…”

Section: Imaging the Parkinsonian Brain: What Have We Learned About Tmentioning

confidence: 99%

Imaging of Motor Cortex Physiology in Parkinson's Disease

Burciu

Vaillancourt

2018

Movement Disorders

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There is abundant evidence that the pathophysiology of Parkinson's disease (PD) is not confined to the nigrostriatal dopaminergic pathway but propagates along the cortico‐basal ganglia‐thalamo‐cortical neural network. A critical node in this functional circuit impacted by PD is the primary motor cortex (M1), which plays a key role in generating neural impulses that regulate movements. The past several decades have lay witness to numerous in vivo neuroimaging techniques that provide a window into the function and structure of M1. A consistent observation from numerous studies is that during voluntary movement, but also at rest, the functional activity of M1 is altered in PD relative to healthy individuals, and it relates to many of the motor signs. Although this abnormal functional activity can be partially restored with acute dopaminergic medication, it continues to deteriorate with disease progression and may predate structural degeneration of M1. The current review discusses the evidence that M1 is fundamental to the pathophysiology of PD, as measured by neuroimaging techniques such as positron emission tomography, single‐photon emission computed tomography, electroencephalography, magnetoencephalography, and functional and structural MRI. Although novel treatments that target the cortex will not cure PD, they could significantly slow down and alter the progressive course of the disease and thus improve clinical care for this degenerative disease. © 2018 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society

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Section: Imaging the Parkinsonian Brain: What Have We Learned About Tmentioning

confidence: 99%

Imaging of Motor Cortex Physiology in Parkinson's Disease

Burciu

Vaillancourt

2018

Movement Disorders

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“…The study authors concluded that the CTC pathway was not primarily driving the rest tremor. However, in another study by Lefaivre et al, rest tremor as rated by kinematic parameters was reduced by lowfrequency rTMS targeted to the medial and lateral cerebellum (43). These two studies used different stimulation techniques and there were differences in clinical populations, which could explain the conflicting results.…”

Section: Therapeutic Use Of Rtmsmentioning

confidence: 97%

Transcranial Magnetic Stimulation in Tremor Syndromes: Pathophysiologic Insights and Therapeutic Role

et al. 2021

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Transcranial magnetic stimulation (TMS) is a painless, non-invasive, and established brain stimulation technique to investigate human brain function. Over the last three decades, TMS has shed insight into the pathophysiology of many neurological disorders. Tremor is an involuntary, rhythmic oscillatory movement disorder commonly related to pathological oscillations propagated via the cerebello-thalamo-cortical pathway. Although tremor is the most common movement disorder and recent imaging studies have enhanced our understanding of the critical pathogenic networks, the underlying pathophysiology of different tremor syndromes is complex and still not fully understood. TMS has been used as a tool to further our understanding of tremor pathophysiology. In addition, repetitive TMS (rTMS) that can modulate brain functions through plasticity effects has been targeted to the tremor network to gain potential therapeutic benefits. However, evidence is available for only a few studies that included small patient samples with limited clinical follow-up. This review aims to discuss the role of TMS in advancing the pathophysiological understanding as well as emerging applications of rTMS for treating individual tremor syndromes. The review will focus on essential tremor, Parkinson's disease tremor, dystonic tremor syndrome, orthostatic tremor, and functional tremor.

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“…This may have been due to additional thalamic and cerebellar dysfunctions in these patients that could act as compensatory mechanisms which curb the effects of nigrostriatal depletion, thereby masking parkinsonism features 42 . Indeed, both thalamic and cerebellar inhibition has been shown to improve features such as tremor in PD patients 75,76 . These, and perhaps other compensatory mechanisms, may become ineffective at a more advanced stage of disease and ultimately result in a parkinsonism phenotype in some cases.…”

Section: Mtdna Maintenance Genes As Pd Risk Factorsmentioning

confidence: 99%

Nuclear Genes Associated with Mitochondrial DNA Processes as Contributors to Parkinson's Disease Risk

et al. 2021

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Over the past four decades, mitochondrial dysfunction has been a recurring theme in Parkinson's disease (PD) and is hypothesized to play a central role in its disease pathogenesis. Given the instrumental role of mitochondria in cellular energy production, their dysfunction can be detrimental to highly energy‐dependent dopaminergic neurons, known to degenerate in PD. Mitochondria harbor multiple copies of their own genomes (mtDNA), encoding critical respiratory chain complexes required for energy production. Consequently, mtDNA has been investigated as a source of mitochondrial dysfunction in PD. As seen in multiple mitochondrial diseases, deleterious mtDNA variation and mtDNA copy number depletion can impede mtDNA protein synthesis, leading to inadequate energy production in affected cells and the onset of a disease phenotype. As such, high burdens of mtDNA defects but also mtDNA depletion, previously identified in the substantia nigra of PD patients, have been suggested to play a role in PD. Genetic variation in nuclear DNA encoding factors required for replicating, transcribing, and translating mtDNA, could underlie these observed mtDNA changes. Herein we examine this possibility and provide an overview of studies that have investigated whether nuclear‐encoded genes associated with mtDNA processes may influence PD risk. Overall, pathway‐based analysis studies, mice models, and case reports of mitochondrial disease patients manifesting with parkinsonism all implicate genes encoding factors related to mtDNA processes in neurodegeneration and PD. Most notably, cumulative genetic variation in these genes likely contributes to neurodegeneration and PD risk by acting together in common pathways to disrupt mtDNA processes or impair their regulation. © 2021 International Parkinson and Movement Disorder Society © 2021 International Parkinson and Movement Disorder Society

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Cerebellar involvement in Parkinson’s disease resting tremor

Cited by 18 publications

References 24 publications

Imaging of Motor Cortex Physiology in Parkinson's Disease

Imaging of Motor Cortex Physiology in Parkinson's Disease

Transcranial Magnetic Stimulation in Tremor Syndromes: Pathophysiologic Insights and Therapeutic Role

Nuclear Genes Associated with Mitochondrial DNA Processes as Contributors to Parkinson's Disease Risk

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