<?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%">Anthony T. Cacace</style></author><author><style face="normal" font="default" size="100%">Satya-Murti, S.</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%">Human middle-latency auditory evoked potentials: vertex and temporal components.</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%">(human)</style></keyword><keyword><style  face="normal" font="default" size="100%">middle-latency auditory evoked potential (MLAEP)</style></keyword><keyword><style  face="normal" font="default" size="100%">temporal components</style></keyword><keyword><style  face="normal" font="default" size="100%">vertex components</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1990</style></year><pub-dates><date><style  face="normal" font="default" size="100%">02/1990</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/1688786</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">77</style></volume><pages><style face="normal" font="default" size="100%">6–18</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">We recorded middle-latency (20-70 msec) auditory evoked potentials (MLAEPs) to monaural and binaural clicks in 30 normal adults (ages 20-49 years) at 32 scalp locations all referred to a balanced non-cephalic reference. Our goal was to define the MLAEP components that were present at comparable latencies and comparable locations across the subject population. Group and individual data were evaluated both as topographic maps and as MLAEPs at selected electrode locations. Three major components occurred between 20 and 70 msec, two well-known peaks centered at the vertex, and one previously undefined peak focused over the posterior temporal area. Pa is a 29 msec positive peak centered at the vertex and present with both monaural and binaural stimulation. Pb is a 53 msec positive peak also centered at the vertex but seen consistently only with binaural and right ear stimulation. TP41 is a 41 msec positive peak focused over both temporal areas. TP41 has not been identified in previous MLAEP studies that concentrated on central scalp locations and/or used active reference electrode sites such as ears or mastoids. Available topographic, intracranial, pharmacologic, and lesion studies indicate that Pa, Pb and TP41 are of neural origin. Whether Pa and/or Pb are produced in Heschl's gyrus, primary auditory cortex, remains unclear. TP41 is probably produced by auditory cortex on the posterior lateral surface of the temporal lobe. It should prove of considerable value in experimental and clinical evaluation of higher level auditory function in particular and of cortical function in general.</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%">Dowman, R.</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Seegal, R. F.</style></author><author><style face="normal" font="default" size="100%">Satya-Murti, S.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Chronic exposure of primates to 60-Hz electric and magnetic fields: III. Neurophysiologic effects.</style></title><secondary-title><style face="normal" font="default" size="100%">Bioelectromagnetics</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">60-Hz electromagnetic radiation</style></keyword><keyword><style  face="normal" font="default" size="100%">auditory</style></keyword><keyword><style  face="normal" font="default" size="100%">brainstem auditory</style></keyword><keyword><style  face="normal" font="default" size="100%">evoked potential</style></keyword><keyword><style  face="normal" font="default" size="100%">primates</style></keyword><keyword><style  face="normal" font="default" size="100%">somatosensory</style></keyword><keyword><style  face="normal" font="default" size="100%">visual</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1989</style></year><pub-dates><date><style  face="normal" font="default" size="100%">01/1989</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/2751703</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">10</style></volume><pages><style face="normal" font="default" size="100%">303–317</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The neurophysiologic effects of combined 60-Hz electric (E) and magnetic (B) fields, of magnitudes comparable to those produced by high-voltage powerlines, were investigated in 10 monkeys (Macaca nemestrina). Six animals (experimental group) were each exposed to three different levels of E and B fields: 3 kV/m and 0.1 G, 10 kV/m and 0.3 G, and 30 kV/m and 0.9 G. Field exposures were preceded and followed by sham exposures, during which factors of field generation were present (e.g., heat, vibration, noise, etc.) without E and B fields. Each of the five segments (i.e., the three exposure segments and the initial and final sham exposure segments) lasted 3 weeks. Animals were exposed for 18 h/day (fields on at 1600 h, off at 1000 h). Four other animals (external control group) were given sham exposure for the entire 15-week period. Auditory, visual, and somatosensory evoked potentials were recorded twice a week, during the daily 6-h field-off period. E- and B-field exposure had no effect on the early or mid-latency evoked potential components, suggesting that exposure at these levels has no effect on peripheral or central sensory afferent pathways. However, there was a statistically significant decrease in the amplitudes of late components of the somatosensory evoked potential during the 10kV/m and 0.3 G, and 30 kV/m and 0.9 G exposure levels. This result is possibly related to the opiate antagonist effect of electromagnetic field exposure reported by others.</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%">Anthony T. Cacace</style></author><author><style face="normal" font="default" size="100%">Goldstein, J. C.</style></author><author><style face="normal" font="default" size="100%">Parnes, S. M.</style></author><author><style face="normal" font="default" size="100%">Satya-Murti, S.</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%">Psychoacoustic and electrophysiologic effects of partial eighth nerve damage.</style></title><secondary-title><style face="normal" font="default" size="100%">American journal of otolaryngology</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Vestibulocochlear Nerve Diseases</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%">02/1984</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/6534193</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">5</style></volume><pages><style face="normal" font="default" size="100%">43–48</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The authors present psychoacoustic and electrophysiologic data concerning a patient with partial damage to the auditory nerve, presumably from a dilated arterial vessel. The lesion was described and documented during neurosurgery for vestibular nerve decompression. Pure tone thresholds, psychoacoustical tuning curves, speech reception ability for spondaic words, maximum word recognition performance for monosyllabic NU-6 word lists, and performance on the synthetic sentence identification test in the ipsilateral and contralateral competing message modalities were normal. Findings consistent with eighth nerve dysfunction, absent contralateral acoustic reflexes, absent or unrecognizable early evoked potentials occurring in the first 10 msec, brainstem auditory evoked potentials (BAEPs), and slight rollover of the performance intensity function for monosyllabic words were obtained on the involved side. In spite of the grossly abnormal BAEPs, two late, presumably cortical, auditory evoked potential components, which occur in the 60 to 250-msec range–vertex potential and T complex–were present and normal. The findings indicate that the perceptual processes needed for speech reception and recognition and for the appearance of later, presumably cortical-evoked potentials can be preserved despite partial damage to the auditory nerve.</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%">Satya-Murti, S.</style></author><author><style face="normal" font="default" size="100%">Jonathan Wolpaw</style></author><author><style face="normal" font="default" size="100%">Anthony T. Cacace</style></author><author><style face="normal" font="default" size="100%">Schaffer, C. A.</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Late auditory evoked potentials can occur without brain stem potentials.</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%">Humans</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1983</style></year><pub-dates><date><style  face="normal" font="default" size="100%">10/1983</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/6193943</style></url></web-urls></urls><volume><style face="normal" font="default" size="100%">56</style></volume><pages><style face="normal" font="default" size="100%">304–308</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">The sequence of early, middle and late auditory evoked potentials is well known. However, it is unknown whether the late (60-250 msec) potentials can occur independently of the early, brain stem potentials. Therefore, in 6 subjects with markedly abnormal or absent brain stem potentials, we recorded two of the late potentials: the vertex potential and the T-complex. The latter is a putative product of auditory cortex. Both of these potentials were clearly evident in all patients in spite of the absence of or marked abnormalities in brain stem potentials.</style></abstract></record></records></xml>