Jeffrey D. Riley
University of California, Irvine
17 Papers
46 Citations
Jeffrey D. Riley is an academic researcher from University of California, Irvine. The author has contributed to research in topics: Epilepsy & Temporal lobe. The author has an hindex of 14, co-authored 17 publications. Previous affiliations of Jeffrey D. Riley include University of Iowa.
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Papers
Vulnerability of the frontal-temporal connections in temporal lobe epilepsy.
TL;DR: TLE is associated with abnormal integrity of frontal-temporal white matter tracts, but only on the side of seizure onset, which suggests that frontal- Temporalwhite matter tracts are vulnerable to recurrent seizures and/or the factors precipitating the epilepsy.
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Functional Mechanisms of Recovery after Chronic Stroke: Modeling with the Virtual Brain.
Maria Inez Falcon,Jeffrey D. Riley,Viktor K. Jirsa,Viktor K. Jirsa,Anthony R. McIntosh,E. Elinor Chen,Ana Solodkin +6 more
- 01 Mar 2016
TL;DR: The Virtual Brain reveals a disrupted post-stroke system favoring excitation- over-inhibition and local-over-global dynamics, consistent with existing mammal literature on stroke mechanisms.
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Caudate atrophy and impaired frontostriatal connections are linked to executive dysfunction in temporal lobe epilepsy
TL;DR: The results suggest that atrophy in the dorsal head of the caudate might disrupt frontostriatal networks that are critical for executive functioning in TLE.
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Neural Correlates of Passive Position Finger Sense After Stroke.
Morgan L. Ingemanson,Justin R. Rowe,Vicky Chan,Jeffrey D. Riley,Eric T. Wolbrecht,David J. Reinkensmeyer,Steven C. Cramer +6 more
TL;DR: It is hypothesized that a model incorporating both neural injury and neural function of the somatosensory system is necessary for delineating proprioception deficits poststroke, andMultivariable modeling found that contralesional proprioceptions deficits were best explained by a combination of neural function (connectivity between ipsilesional secondary somatoensory cortex) and neural injury (total sensory system injury).
Ablation of NK1 Receptors in Rat Nucleus Tractus Solitarii Blocks Baroreflexes
TL;DR: Using SP conjugated with the toxin saporin, which kills the neurons at which SP may act, test the hypothesis that neurons expressing the neurokinin-1 receptor are critical to baroreflex transmission in the nucleus tractus solitarii of rat.
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