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Paul C. Van Ness

Researcher at Baylor College of Medicine

Publications -  54
Citations -  3542

Paul C. Van Ness is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: Epilepsy & Temporal lobe. The author has an hindex of 24, co-authored 54 publications receiving 2929 citations. Previous affiliations of Paul C. Van Ness include University of Texas at Austin & University of Texas Southwestern Medical Center.

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Two‐year seizure reduction in adults with medically intractable partial onset epilepsy treated with responsive neurostimulation: Final results of the RNS System Pivotal trial

TL;DR: To demonstrate the safety and effectiveness of responsive stimulation at the seizure focus as an adjunctive therapy to reduce the frequency of seizures in adults with medically intractable partial onset seizures arising from one or two seizure foci.
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Long-term treatment with responsive brain stimulation in adults with refractory partial seizures

TL;DR: This study provides Class IV evidence that for adults with medically refractory partial onset seizures, responsive direct cortical stimulation reduces seizures and improves quality of life over a mean follow-up of 5.4 years.
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Brain-responsive neurostimulation in patients with medically intractable mesial temporal lobe epilepsy

Eric B. Geller, +48 more
- 01 Jun 2017 - 
TL;DR: In this paper, the authors evaluated the seizure-reduction response and safety of brain-responsive stimulation in adults with medically intractable partial-onset seizures of mesial temporal lobe origin.
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Evaluation of Neurologic Function in Gulf War Veterans: A Blinded Case-Control Study

TL;DR: The 3 factor-derived syndromes identified among Gulf War veterans appear to represent variants of a generalized injury to the nervous system.
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Angelman syndrome: Correlations between epilepsy phenotypes and genotypes

TL;DR: In conclusion, maternally inherited chromosome 15q11‐13 deletions produce severe epilepsy in Angelman syndrome, and loss‐of‐function UBE3A mutations, uniparental disomy, or methylation imprint abnormalities in AS are associated with relatively mild epilepsy.