Abstract
that excessive beta synchrony is delayed in its development in toxininduced animal models of parkinsonism. Thus it may not contribute to the earliest deficits. Second, the proof of principle studies showing worsening of bradykinesia with stimulation of the basal ganglia at beta band frequencies in patients have only produced mild, albeit significant, worsening. The latter brings in to question the quantitive importance of beta synchrony in bradykinesia and rigidity. Still, its value as a biomarker in parkinsonism seems strong, and as such it could be used as a surrogate measure of efficacy in animal models of parkinsonism and as a feedback signal in closed-loop deep bran stimulation systems.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
