Unravelling delayed therapy escape after thalamic deep brain stimulation for essential tremor? - Additional clinical and neuroimaging evidence.
Deep brain stimulation
Delayed therapy escape
Essential tremor
Habituation
PET
Journal
NeuroImage. Clinical
ISSN: 2213-1582
Titre abrégé: Neuroimage Clin
Pays: Netherlands
ID NLM: 101597070
Informations de publication
Date de publication:
2022
2022
Historique:
received:
27
02
2022
revised:
15
07
2022
accepted:
08
08
2022
pubmed:
22
8
2022
medline:
15
12
2022
entrez:
21
8
2022
Statut:
ppublish
Résumé
Delayed therapy escape after thalamic deep brain stimulation (DBS) for essential tremor is a serious yet frequent condition. It is often difficult to detect this process at onset due to its gradual evolution. Here we aim to identify clinical and neuroimaging hallmarks of delayed therapy escape. We retrospectively studied operationalized and quantitative analyses of tremor and gait, as well as [ Of the immediately accessible parametric tremor data (i.e. ON or OFF Rebound frequency of postural tremor seems to be a good diagnostic marker for delayed therapy escape. Regional glucose metabolism suggests that this phenomenon may be associated with increased metabolic activity in the thalamus and dentate nucleus possibly due to antidromic stimulation effects. We see reasons to interpret the delayed therapy escape phenomenon as being related to long term and chronic DBS.
Sections du résumé
BACKGROUND
BACKGROUND
Delayed therapy escape after thalamic deep brain stimulation (DBS) for essential tremor is a serious yet frequent condition. It is often difficult to detect this process at onset due to its gradual evolution.
OBJECTIVE
OBJECTIVE
Here we aim to identify clinical and neuroimaging hallmarks of delayed therapy escape.
METHODS
METHODS
We retrospectively studied operationalized and quantitative analyses of tremor and gait, as well as [
RESULTS
RESULTS
Of the immediately accessible parametric tremor data (i.e. ON or OFF
CONCLUSIONS
CONCLUSIONS
Rebound frequency of postural tremor seems to be a good diagnostic marker for delayed therapy escape. Regional glucose metabolism suggests that this phenomenon may be associated with increased metabolic activity in the thalamus and dentate nucleus possibly due to antidromic stimulation effects. We see reasons to interpret the delayed therapy escape phenomenon as being related to long term and chronic DBS.
Identifiants
pubmed: 35988341
pii: S2213-1582(22)00215-7
doi: 10.1016/j.nicl.2022.103150
pmc: PMC9402391
pii:
doi:
Substances chimiques
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
103150Informations de copyright
Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: BEAS receives a research grant from Ceregate (Hamburg, Germany) unrelated to this publication. NS received a grant from the Berta-Ottenstein-Programme for Clinician Scientists, Faculty of Medicine,University of Freiburg, and received payment for a lecture sponsored by Abbvie. PCR receives research support from: Else Kröner-Fresenius Foundation (Germany) and Fraunhofer Foundation (Germany). He is a consultant for Boston Scientific (USA), Inomed (Germany) and Brainlab (Germany). JB received a grant from the German Research Foundation (Deutsche Forschungsgemeinschaft, DFG). PTM received honoraria from GE (presentation, consultancy) and Philips (presentation). VAC receives a collaborative grant from BrainLab (Munich, Germany). He is a consultant for Ceregate (Hamburg, Germany), Cortec (Freiburg, Germany) and Inbrain (Barcelona, Spain). He has ongoing IITs with Medtronic (USA) and Boston Scientific (USA). GB, IW, CM, MLF, MR, TP, have nothing to report. All declared interests are outside of the submitted work.