Central thalamic deep-brain stimulation in the severely injured brain: rationale and proposed mechanisms of action.

TitleCentral thalamic deep-brain stimulation in the severely injured brain: rationale and proposed mechanisms of action.
Publication TypeJournal Article
Year of Publication2009
AuthorsSchiff, Nicholas D.
JournalAnn N Y Acad Sci
Volume1157
Pagination101-16
Date Published2009 Mar
ISSN1749-6632
KeywordsAdult, Arousal, Brain Injuries, Consciousness Disorders, Deep Brain Stimulation, Humans, Male, Nerve Net, Prosencephalon, Thalamus
Abstract

This review outlines the scientific rationale supporting the potential use of deep-brain electrical stimulation (DBS) in the central thalamus as a method to improve behavioral responsiveness following severe brain injury. Neurons within the central thalamus are selectively vulnerable to disconnection and dysfunction following severe brain injuries because of their unique geometry of cerebral connections. Because the central thalamus plays a key role in forebrain arousal regulation, impaired function of these cells has a broad impact. Prior clinical investigations, however, have targeted some components of the thalamus and related subcortical structures to improve behavioral responsiveness after severe brain injuries without providing evidence of sustained and clinically meaningful behavioral effects. Here important differences in conceptual framework, consideration of diagnostic categories for patient selection, and anticipated mechanisms of effect that distinguish earlier approaches and current studies are reviewed. As opposed to targeting chronically unresponsive patients, current efforts focus on identification of conscious patients with significant preservation of large-scale integrative cerebral networks. The potential mechanisms and limitations of this evolving strategy are discussed, including the need to develop frameworks to calibrate patient selection to potential clinical benefits, range of potential effect size, and other present unknowns.

DOI10.1111/j.1749-6632.2008.04123.x
Alternate JournalAnn. N. Y. Acad. Sci.
PubMed ID19351360

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