Modified Fluorodeoxyglucose Metabolism in Motor Circuitry by Subthalamic Deep Brain Stimulation

Cao, Chunyan; Zhang, Huiwei; Li, Dianyou; Zhan, Siyan; Zhang, Jing; Zhang, Xiaoxiao; Zuo, Chuantao; Sun, Bomin

doi:10.1159/000455930

Cited by 15 publications

(8 citation statements)

References 20 publications

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“…After 1 year STN DBS treatment, Cao et al . () found ‘pronounced elevations (activation) in parietal and occipital glucose’ plus ‘an obvious reduction in caudate, putamen, cerebellum, and frontal cortex glucose metabolism’.…”

Section: Mechanisms Of Action Of Dbs: a Brief Excursusmentioning

confidence: 99%

Mechanisms of action underlying the efficacy of deep brain stimulation of the subthalamic nucleus in Parkinson's disease: central role of disease severity

Cerroni

Mazzone

Liguori

et al. 2018

Eur J of Neuroscience

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Despite consensus on some neurophysiological hallmarks of the Parkinsonian state (such as beta) band increase) a single mechanism is unlikely to explain the efficacy of deep brain stimulation (DBS) of the subthalamic nucleus (STN). Most experimental evidence to date correlates with an extreme degree of nigral neurodegeneration and not with different stages of PD progression. It seems inappropriate to combine substantially different patients - newly diagnosed, early fluctuators or advanced dyskinetic individuals - within the same group. An efficacious STN-DBS imposes a new activity pattern within brain circuits, favouring alpha- and gamma-like neuronal discharge, and restores the thalamo-cortical transmission pathway through axonal activation. In addition, stimulation via the dorsal contacts of the macro-electrode may affect cortical activation antidromically. However, basal ganglia (BG) modulation remains cardinal for 'OFF'-'ON' transition (as revealed by cGMP increase occurring during STN-DBS in the substantia nigra pars reticulata and internal globus pallidus). New research promises to clarify to what extent STN-DBS restores striato-centric bidirectional plasticity, and whether non-neuronal cellular actions (microglia, neurovascular) play a part. Future studies will assess whether extremely anticipated DBS or lesioning in selected patients are capable of providing neuroprotection to the synuclein-mediated alterations of synaptic efficiency. This review addresses these open issues through the specific mechanisms prevailing in a given disease stage. In patients undergoing early protocol, alteration in endogenous transmitters and recovery of plasticity are concurrent players. In advanced stages, re-modulation of endogenous band frequencies, disruption of pathological pattern and/or antidromic cortical activation are, likely, the prominent modes.

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Section: Mechanisms Of Action Of Dbs: a Brief Excursusmentioning

confidence: 99%

Mechanisms of action underlying the efficacy of deep brain stimulation of the subthalamic nucleus in Parkinson's disease: central role of disease severity

Cerroni

Mazzone

Liguori

et al. 2018

Eur J of Neuroscience

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“…In general, connectivity with subcortical areas (thalamus, midbrain, pons) is diminished, whereas both decreases and increases for different cortico-striatal connections have been reported (Hacker et al, 2012; Hou et al, 2016; Manza et al, 2016). Conflicting results about the effects of STN-DBS emerged from imaging studies: some authors reported STN-DBS-related activations of the striatum (Geday et al, 2009; Hilker et al, 2004; Knight et al, 2015; Stefurak et al, 2003), whereas others found deactivations (Cao et al, 2017; Le Jeune et al, 2010). The impact of STN-DBS on striatal connectivity is entirely unknown.…”

Section: Introductionmentioning

confidence: 99%

Effects of subthalamic deep brain stimulation on striatal metabolic connectivity in a rat hemiparkinsonian model

Apetz

Kordys

Simon

et al. 2019

Disease Models &Amp; Mechanisms

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Deep brain stimulation (DBS) in the subthalamic nucleus (STN) has been successfully used for the treatment of advanced Parkinson's disease, although the underlying mechanisms are complex and not well understood. There are conflicting results about the effects of STN-DBS on neuronal activity of the striatum, and its impact on functional striatal connectivity is entirely unknown. We therefore investigated how STN-DBS changes cerebral metabolic activity in general and striatal connectivity in particular. We used ipsilesional STN stimulation in a hemiparkinsonian rat model in combination with [ 18 F]FDOPA-PET, [ 18 F]FDG-PET and metabolic connectivity analysis. STN-DBS reversed ipsilesional hypometabolism and contralesional hypermetabolism in hemiparkinsonian rats by increasing metabolic activity in the ipsilesional ventrolateral striatum and by decreasing it in the contralesional hippocampus and brainstem. Other STN-DBS effects were subject to the magnitude of dopaminergic lesion severity measured with [ 18 F]FDOPA-PET, e.g. activation of the infralimbic cortex was negatively correlated to lesion severity. Connectivity analysis revealed that, in healthy control animals, left and right striatum formed a bilateral functional unit connected by shared cortical afferents, which was less pronounced in hemiparkinsonian rats. The healthy striatum was metabolically connected to the ipsilesional substantia nigra in hemiparkinsonian rats only (OFF condition). STN-DBS (ON condition) established a new functional striatal network, in which interhemispheric striatal connectivity was strengthened, and both the dopamine-depleted and the healthy striatum were functionally connected to the healthy substantia nigra. We conclude that both unilateral dopamine depletion and STN-DBS affect the whole brain and alter complex interhemispheric networks.

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“…Most importantly, our analysis revealed that this sweet spot, described with relatively high consistency in the literature, might correspond to the SMA cluster. SMA glucose utilization, and hence activity, has been shown to be decreased as an effect of DBS for PD [30].…”

Section: Discussionmentioning

confidence: 99%

Parcellation of the Subthalamic Nucleus in Parkinson’s Disease: A Retrospective Analysis of Atlas- and Diffusion-Based Methods

Zolal

Polanski

Klingelhoefer

et al. 2020

Stereotact Funct Neurosurg

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Background: Deep brain stimulation (DBS) is an established method of treatment for Parkinson's disease (PD). A stimulation sweet spot at the interface between the motor and associative clusters of the subthalamic nucleus (STN) has recently been postulated. The aim of this study was to analyze the available clustering methods for the STN and their correlation to outcome. Methods: This is a retrospective analysis of a group of 20 patients implanted with a DBS device for PD. Atlas-based and diffusion tractography-based parcellation of the STN was performed. The distances of the electrode to the obtained clusters were compared to each other and to outcome parameters, which included levodopa equivalent dose (LED) reduction, Unified Parkinson's Disease Rating Scale (UPDRS)-III scores, and reduction in scores for items 32 and 36 of the UPDRS-IV. Results: The implanted electrodes were located nearest to the motor clusters of the STN. The following significant associations with postoperative LED reduction were found: (1) distance of the electrode to the motor cluster in the Accolla and DISTAL atlases (p < 0.01) and (2) distance of the electrode to the supplementary motor area cluster (p = 0.02). There was no association with either the UPDRS-III or the UPDRS-IV score. Conclusions: The results of this study suggest the possibility that atlas-based clustering, as well as diffusion tractography-based parcellation, can be useful in estimating the stimulation target ("sweet spot") for STN-DBS in PD patients. Atlas-based as well as diffusion-based clustering might become a useful tool in DBS trajectory planning.

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Modified Fluorodeoxyglucose Metabolism in Motor Circuitry by Subthalamic Deep Brain Stimulation

Cited by 15 publications

References 20 publications

Mechanisms of action underlying the efficacy of deep brain stimulation of the subthalamic nucleus in Parkinson's disease: central role of disease severity

Mechanisms of action underlying the efficacy of deep brain stimulation of the subthalamic nucleus in Parkinson's disease: central role of disease severity

Effects of subthalamic deep brain stimulation on striatal metabolic connectivity in a rat hemiparkinsonian model

Parcellation of the Subthalamic Nucleus in Parkinson’s Disease: A Retrospective Analysis of Atlas- and Diffusion-Based Methods

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