<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Kubánek, J</style></author><author><style face="normal" font="default" size="100%">Miller, John W</style></author><author><style face="normal" font="default" size="100%">Ojemann, J G</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Gerwin Schalk</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Decoding flexion of individual fingers using electrocorticographic signals in humans.</style></title><secondary-title><style face="normal" font="default" size="100%">J Neural Eng</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Neural Eng</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Biomechanics</style></keyword><keyword><style  face="normal" font="default" size="100%">Brain</style></keyword><keyword><style  face="normal" font="default" size="100%">Electrodiagnosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Epilepsy</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Fingers</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Microelectrodes</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Motor Activity</style></keyword><keyword><style  face="normal" font="default" size="100%">Rest</style></keyword><keyword><style  face="normal" font="default" size="100%">Thumb</style></keyword><keyword><style  face="normal" font="default" size="100%">Time Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2009</style></year><pub-dates><date><style  face="normal" font="default" size="100%">12/2009</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/19794237</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">6</style></volume><pages><style face="normal" font="default" size="100%">066001</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;span style=&quot;font-family: arial, helvetica, clean, sans-serif; font-size: 13px; line-height: 17px;&quot;&gt;Brain signals can provide the basis for a non-muscular communication and control system, a brain-computer interface (BCI), for people with motor disabilities. A common approach to creating BCI devices is to decode kinematic parameters of movements using signals recorded by intracortical microelectrodes. Recent studies have shown that kinematic parameters of hand movements can also be accurately decoded from signals recorded by electrodes placed on the surface of the brain (electrocorticography (ECoG)). In the present study, we extend these results by demonstrating that it is also possible to decode the time course of the flexion of individual fingers using ECoG signals in humans, and by showing that these flexion time courses are highly specific to the moving finger. These results provide additional support for the hypothesis that ECoG could be the basis for powerful clinically practical BCI systems, and also indicate that ECoG is useful for studying cortical dynamics related to motor function.&lt;/span&gt;&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Xiang Yang Chen</style></author><author><style face="normal" font="default" size="100%">Pillai, Shreejith</style></author><author><style face="normal" font="default" size="100%">Yi Chen</style></author><author><style face="normal" font="default" size="100%">Wang, Yu</style></author><author><style face="normal" font="default" size="100%">Lu Chen</style></author><author><style face="normal" font="default" size="100%">Jonathan S. Carp</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Spinal and supraspinal effects of long-term stimulation of sensorimotor cortex in rats.</style></title><secondary-title><style face="normal" font="default" size="100%">Journal of neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Time Factors</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2007</style></year><pub-dates><date><style  face="normal" font="default" size="100%">08/2007</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/17522179</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">98</style></volume><pages><style face="normal" font="default" size="100%">878–887</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Sensorimotor cortex (SMC) modifies spinal cord reflex function throughout life and is essential for operant conditioning of the H-reflex. To further explore this long-term SMC influence over spinal cord function and its possible clinical uses, we assessed the effect of long-term SMC stimulation on the soleus H-reflex. In freely moving rats, the soleus H-reflex was measured 24 h/day for 12 wk. The soleus background EMG and M response associated with H-reflex elicitation were kept stable throughout. SMC stimulation was delivered in a 20-day-on/20-day-off/20-day-on protocol in which a train of biphasic 1-ms pulses at 25 Hz for 1 s was delivered every 10 s for the on-days. The SMC stimulus was automatically adjusted to maintain a constant descending volley. H-reflex size gradually increased during the 20 on-days, stayed high during the 20 off-days, and rose further during the next 20 on-days. In addition, the SMC stimulus needed to maintain a stable descending volley rose steadily over days. It fell during the 20 off-days and rose again when stimulation resumed. These results suggest that SMC stimulation, like H-reflex operant conditioning, induces activity-dependent plasticity in both the brain and the spinal cord and that the plasticity responsible for the H-reflex increase persists longer after the end of SMC stimulation than that underlying the change in the SMC response to stimulation.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Maniccia, D. M.</style></author><author><style face="normal" font="default" size="100%">Elia, T.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Operant conditioning of primate H-reflex: phases of development.</style></title><secondary-title><style face="normal" font="default" size="100%">Neuroscience letters</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Time Factors</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1994</style></year><pub-dates><date><style  face="normal" font="default" size="100%">04/1994</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/8058188</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">170</style></volume><pages><style face="normal" font="default" size="100%">203–207</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">This study sought to determine whether operantly conditioned change in the primate triceps surae (TS) H-reflex develops in distinct phases. Data from 20 animals in which the TS H-reflex in one leg was trained up (i.e., HRup mode) and 18 in which it was trained down (i.e., HRdown mode) were averaged to define H-reflex behavior in trained and control legs. In HRup animals, the trained-leg H-reflex showed a large phase I increase in the first two days followed by gradual phase II increase that continued for weeks. The control-leg H-reflex appeared to show much smaller phase I and phase II increases. In HRdown animals, the trained-leg H-reflex decreased gradually over weeks, while the control-leg H-reflex appeared to increase within 2 days and did not change from then on. The initial rapid increase in the HRdown control leg suggested that two early events occurred in the HRdown trained leg: a nonspecific increase like that in the control leg and an operantly conditioned mode-specific decrease. These two effects may have obscured each other, so that H-reflex size in the HRdown trained leg did not drop rapidly in the first few days. These results improve understanding of adaptive H-reflex change as an operantly conditioned phenomenon, and provide encouragement and direction for efforts to reproduce and study the phenomenon in reduced or anesthetized preparations.</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">O'Keefe, J. A.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Adaptive plasticity in the primate spinal stretch reflex: evidence for a two-phase process.</style></title><secondary-title><style face="normal" font="default" size="100%">The Journal of neuroscience : the official journal of the Society for Neuroscience</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Time Factors</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1984</style></year><pub-dates><date><style  face="normal" font="default" size="100%">11/1984</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/6502200</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">4</style></volume><pages><style face="normal" font="default" size="100%">2718–2724</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Monkeys can slowly increase or decrease the amplitude of the purely spinal, largely monosynaptic portion of the response to sudden muscle stretch, the spinal stretch reflex (SSR), when confronted by a task requiring such change (Wolpaw, J.R., V.A. Kieffer, R.F. Seegal, D.J. Braitman, and M.G. Sanders (1983) Brain Res. 267: 196-200; Wolpaw, J.R., D.J. Braitman, and R.F. Seegal (1983) J. Neurophysiol. 50: 1296-1311). Change occurs without alteration in initial muscle length or in background activity of agonist, antagonist, or synergist muscles. This study uses composite curves to describe in detail the development of SSR amplitude change. It reveals important, previously unexpected features of this development. SSR increase or decrease appears to occur in two distinct phases. Phase I, a nearly immediate 8% change, occurs within the first 6 hr. Phase II, a 2%/day change, continues for at least 2 months. Although phase II is much slower than phase I, its final magnitude is far greater. Phase I indicates a nearly immediate change in suprasegmental influence of the segmental arc of the SSR. Because stretch onset time is unpredictable and the SSR occurs before any other possible response, this change in descending activity must be tonic; it must be present continually, day after day, for the 5 to 7 hr/day the animal spends at the task. Phase I produces a rapid and significant increase in reward probability. Thus, it may be readily interpreted as an example of operant conditioning, provoked by the reward contingency.(ABSTRACT TRUNCATED AT 250 WORDS)</style></abstract></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Penry, J. K.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A temporal component of the auditory evoked response.</style></title><secondary-title><style face="normal" font="default" size="100%">Electroencephalography and clinical neurophysiology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Time Factors</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1975</style></year><pub-dates><date><style  face="normal" font="default" size="100%">12/1975</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/53139</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">39</style></volume><pages><style face="normal" font="default" size="100%">609–620</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">We studied the 75-225 msec portion of the auditory evoked response (AER) in 32 normal adults at vertex (Cz) and temporal (T3 and T4) placements referred to a balanced, noncephalic reference electrode using a monaural 1 msec click stimulus delivered every 4.7 sec at 60 dB above threshold. The tape-recorded EEG was filtered at 1-25 c/sec, and 128 individual responses were summed, sampling every 0.5 msec for 250 msec post-stimulation. The Cz AERs showed the classic vertex response, a negative peak, N1, at 100 msec, followed by a positive peak, P2, at 160-200 msec. The T3 and T4 AERs were similar to the Cz AERs from 0 to 80 msec and from 200 to 250 msec. They differed significantly from the Cz AERs from 80 to 200 msec. The difference is best explained by the hypothesis that the Cz AERs consisted of N1P2, while the T3 and T4 AERs consisted of N1P2 plus an additional superimposed component, which we called the T complex, comprising a positive peak, Ta, at 105-110 msec, and a negative peak, Tb, at 150-160 msec. By computer, the corresponding Cz and T3 or T4 AERs were normalized to equalize their amplitudes, and the former was subtracted from the latter, thus isolating the T complex. The Ta peak was found to occur 1.5 +/- 1.6 msec earlier at the electrode contralateral to stimulation, and 2.2 +/- 4.0 msec earlier at the T4 (right) electrode. Both differences were statistically significant. The T complex amplitude was greater at the electrode contralateral to stimulation and at the T4 electrode. These findings appear to resolve current controversies concerning the form of the temporal AER. While N1P2 is apparently a product of widespread areas of cortex, we conclude that the T complex is probably a product of secondary auditory cortex.</style></abstract></record></records></xml>