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Coralie de Hemptinne

Researcher at University of California, San Francisco

Publications -  60
Citations -  3425

Coralie de Hemptinne is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Deep brain stimulation & Subthalamic nucleus. The author has an hindex of 24, co-authored 50 publications receiving 2370 citations. Previous affiliations of Coralie de Hemptinne include University of California, Berkeley & United States Department of Veterans Affairs.

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Therapeutic deep brain stimulation reduces cortical phase-amplitude coupling in Parkinson's disease

TL;DR: It is proposed that DBS of the basal ganglia improves cortical function by alleviating excessive beta phase locking of motor cortex neurons.
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Exaggerated phase–amplitude coupling in the primary motor cortex in Parkinson disease

TL;DR: Analysis of local field potentials recorded from the primary motor cortex (M1) arm area in patients undergoing neurosurgery prompts a model of the basal ganglia–cortical circuit in Parkinson disease incorporating phase–amplitude interactions and abnormal corticosubthalamic feedback.
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Adaptive deep brain stimulation for Parkinson's disease using motor cortex sensing.

TL;DR: This is the first demonstration of adaptive DBS in Parkinson's disease using a fully implanted device and neural sensing, and the approach is distinct from other strategies utilizing basal ganglia signals for feedback control.
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Gamma Oscillations in the Hyperkinetic State Detected with Chronic Human Brain Recordings in Parkinson's Disease

TL;DR: This work characterized an oscillation between cortex and subcortical modulators that is associated with a serious adverse effect of therapy for Parkinson's disease: dyskinesia and suggests a possible biomarker for feedback-controlled neurostimulation to treat hyperkinetic disorders.
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Nonsinusoidal beta oscillations reflect cortical pathophysiology in Parkinson's disease

TL;DR: The results suggest that the pathophysiological beta generator is altered by DBS, smoothing out the beta waveform, which has implications not only for the interpretation of the physiological mechanism by which DBS reduces PD-related motor symptoms, but more broadly for the analytic toolkit in general.