Basal Ganglia Pathways Associated With Therapeutic Pallidal Deep Brain Stimulation for Tourette Syndrome.

Deep Brain Stimulation Globus Pallidus Humans Retrospective Studies Tourette Syndrome / therapy Treatment Outcome
Computational model Globus pallidus internus Internal capsule Obsessive-compulsive behavior Pallido-subthalamic Tics

Journal

Biological psychiatry. Cognitive neuroscience and neuroimaging
ISSN: 2451-9030
Titre abrégé: Biol Psychiatry Cogn Neurosci Neuroimaging
Pays: United States
ID NLM: 101671285

Informations de publication

Date de publication:
10 2021
Historique:
received: 25 08 2020
revised: 28 10 2020
accepted: 14 11 2020
pubmed: 5 2 2021
medline: 3 11 2021
entrez: 4 2 2021
Statut: ppublish

Résumé

Deep brain stimulation (DBS) targeting the globus pallidus internus (GPi) can improve tics and comorbid obsessive-compulsive behavior (OCB) in patients with treatment-refractory Tourette syndrome (TS). However, some patients' symptoms remain unresponsive, the stimulation applied across patients is variable, and the mechanisms underlying improvement are unclear. Identifying the fiber pathways surrounding the GPi that are associated with improvement could provide mechanistic insight and refine targeting strategies to improve outcomes. Retrospective data were collected for 35 patients who underwent bilateral GPi DBS for TS. Computational models of fiber tract activation were constructed using patient-specific lead locations and stimulation settings to evaluate the effects of DBS on basal ganglia pathways and the internal capsule. We first evaluated the relationship between activation of individual pathways and symptom improvement. Next, linear mixed-effects models with combinations of pathways and clinical variables were compared in order to identify the best-fit predictive models of tic and OCB improvement. The best-fit model of tic improvement included baseline severity and the associative pallido-subthalamic pathway. The best-fit model of OCB improvement included baseline severity and the sensorimotor pallido-subthalamic pathway, with substantial evidence also supporting the involvement of the prefrontal, motor, and premotor internal capsule pathways. The best-fit models of tic and OCB improvement predicted outcomes across the cohort and in cross-validation. Differences in fiber pathway activation likely contribute to variable outcomes of DBS for TS. Computational models of pathway activation could be used to develop novel approaches for preoperative targeting and selecting stimulation parameters to improve patient outcomes.

Sections du résumé

BACKGROUND
Deep brain stimulation (DBS) targeting the globus pallidus internus (GPi) can improve tics and comorbid obsessive-compulsive behavior (OCB) in patients with treatment-refractory Tourette syndrome (TS). However, some patients' symptoms remain unresponsive, the stimulation applied across patients is variable, and the mechanisms underlying improvement are unclear. Identifying the fiber pathways surrounding the GPi that are associated with improvement could provide mechanistic insight and refine targeting strategies to improve outcomes.
METHODS
Retrospective data were collected for 35 patients who underwent bilateral GPi DBS for TS. Computational models of fiber tract activation were constructed using patient-specific lead locations and stimulation settings to evaluate the effects of DBS on basal ganglia pathways and the internal capsule. We first evaluated the relationship between activation of individual pathways and symptom improvement. Next, linear mixed-effects models with combinations of pathways and clinical variables were compared in order to identify the best-fit predictive models of tic and OCB improvement.
RESULTS
The best-fit model of tic improvement included baseline severity and the associative pallido-subthalamic pathway. The best-fit model of OCB improvement included baseline severity and the sensorimotor pallido-subthalamic pathway, with substantial evidence also supporting the involvement of the prefrontal, motor, and premotor internal capsule pathways. The best-fit models of tic and OCB improvement predicted outcomes across the cohort and in cross-validation.
CONCLUSIONS
Differences in fiber pathway activation likely contribute to variable outcomes of DBS for TS. Computational models of pathway activation could be used to develop novel approaches for preoperative targeting and selecting stimulation parameters to improve patient outcomes.

Identifiants

DOI: 10.1016/j.bpsc.2020.11.005 PMID: 33536144 PMC: PMC8864935
pubmed: 33536144
pii: S2451-9022(20)30347-5
doi: 10.1016/j.bpsc.2020.11.005
pmc: PMC8864935
mid: NIHMS1668704
pii:
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

961-972

Subventions

Organisme : NIGMS NIH HHS
ID : P41 GM103545
Pays : United States
Organisme : NINR NIH HHS
ID : R01 NR014852
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS096008
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2020 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

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Auteurs

Kara A Johnson (KA)

Scientific Computing and Imaging Institute, University of Utah, Salt Lake City, Utah; Department of Biomedical Engineering, University of Utah, Salt Lake City, Utah.

Gordon Duffley (G)

Scientific Computing and Imaging Institute, University of Utah, Salt Lake City, Utah; Department of Biomedical Engineering, University of Utah, Salt Lake City, Utah.

Thomas Foltynie (T)

Functional Neurosurgery Unit, Department of Clinical and Movement Neurosciences, Queen Square Institute of Neurology, University College London, London, United Kingdom.

Marwan Hariz (M)

Functional Neurosurgery Unit, Department of Clinical and Movement Neurosciences, Queen Square Institute of Neurology, University College London, London, United Kingdom; Department of Clinical Neuroscience, Umea University, Umea, Sweden.

Ludvic Zrinzo (L)

Functional Neurosurgery Unit, Department of Clinical and Movement Neurosciences, Queen Square Institute of Neurology, University College London, London, United Kingdom.

Eileen M Joyce (EM)

Functional Neurosurgery Unit, Department of Clinical and Movement Neurosciences, Queen Square Institute of Neurology, University College London, London, United Kingdom.

Harith Akram (H)

Functional Neurosurgery Unit, Department of Clinical and Movement Neurosciences, Queen Square Institute of Neurology, University College London, London, United Kingdom.

Domenico Servello (D)

Neurosurgical Department, IRCCS Istituto Ortopedico Galeazzi, Milan, Italy.

Tommaso F Galbiati (TF)

Neurosurgical Department, IRCCS Istituto Ortopedico Galeazzi, Milan, Italy.

Alberto Bona (A)

Neurosurgical Department, IRCCS Istituto Ortopedico Galeazzi, Milan, Italy.

Mauro Porta (M)

Tourette's Syndrome and Movement Disorders Center, IRCCS Istituto Ortopedico Galeazzi, Milan, Italy.

Fan-Gang Meng (FG)

Beijing Neurosurgical Institute, Capital Medical University, Beijing, China.

Albert F G Leentjens (AFG)

Department of Psychiatry and Neuropsychology, Maastricht University Medical Centre, Maastricht, the Netherlands.

Aysegul Gunduz (A)

Norman Fixel Institute for Neurological Diseases, Program for Movement Disorders and Neurorestoration, Departments of Neurology and Neurosurgery, University of Florida, Gainesville, Florida; J. Crayton Pruitt Family Department of Biomedical Engineering, University of Florida, Gainesville, Florida.

Wei Hu (W)

Norman Fixel Institute for Neurological Diseases, Program for Movement Disorders and Neurorestoration, Departments of Neurology and Neurosurgery, University of Florida, Gainesville, Florida.

Kelly D Foote (KD)

Norman Fixel Institute for Neurological Diseases, Program for Movement Disorders and Neurorestoration, Departments of Neurology and Neurosurgery, University of Florida, Gainesville, Florida.

Michael S Okun (MS)

Norman Fixel Institute for Neurological Diseases, Program for Movement Disorders and Neurorestoration, Departments of Neurology and Neurosurgery, University of Florida, Gainesville, Florida.

Christopher R Butson (CR)

Scientific Computing and Imaging Institute, University of Utah, Salt Lake City, Utah; Department of Biomedical Engineering, University of Utah, Salt Lake City, Utah; Department of Neurology, University of Utah, Salt Lake City, Utah; Department of Neurosurgery, University of Utah, Salt Lake City, Utah; Department of Psychiatry, University of Utah, Salt Lake City, Utah. Electronic address: butson@sci.utah.edu.

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Classifications MeSH

questionsmedicales.fr › Procédures de chirurgie opératoire › Stimulation cérébrale profonde › Basal Ganglia Pathways Associated With...
questionsmedicales.fr › Système nerveux › Système nerveux central › Encéphale › Prosencéphale › Télencéphale › Cerveau › Noyaux gris centraux › Corps strié › Globus pallidus › Basal Ganglia Pathways Associated With...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Primates › Haplorhini › Catarrhini › Hominidae › Humains › Basal Ganglia Pathways Associated With...
questionsmedicales.fr › Environnement et santé publique › Santé publique › Méthodes épidémiologiques › Caractéristiques des études épidémiologiques › Études épidémiologiques › Études de cohortes › Études rétrospectives › Basal Ganglia Pathways Associated With...
questionsmedicales.fr › Troubles mentaux › Troubles du développement neurologique › Troubles des tics › Syndrome de Tourette › Basal Ganglia Pathways Associated With...
questionsmedicales.fr › Qualité, accès, évaluation des soins de santé › Qualité des soins de santé › Mécanismes d'évaluation des soins de santé › Évaluation des résultats et des processus en soins de santé › Évaluation de résultat (soins) › Résultat thérapeutique › Basal Ganglia Pathways Associated With...