02290nas a2200217   4500008004100000022001400041245008500055210006900140260001200209300001100221490000700232520161000239653001201849653005301861653002401914653002201938100002401960700002001984700002102004856004702025       1990                        eng d  a0013-469400aHuman middle-latency auditory evoked potentials: vertex and temporal components.0 aHuman middlelatency auditory evoked potentials vertex and tempor  c02/1990  a6–180 v773 aWe 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.10a(human)10amiddle-latency auditory evoked potential (MLAEP)10atemporal components10avertex components1 aCacace, Anthony, T.1 aSatya-Murti, S.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/168878602268nas a2200265   4500008004100000022001400041245010300055210006900158260001200227300001400239490000700253520148500260653003601745653001301781653002301794653002101817653001301838653001801851653001101869100001501880700002101895700001901916700002001935856004701955       1989                        eng d  a0197-846200aChronic exposure of primates to 60-Hz electric and magnetic fields: III. Neurophysiologic effects.0 aChronic exposure of primates to 60Hz electric and magnetic field  c01/1989  a303–3170 v103 aThe 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.10a60-Hz electromagnetic radiation10aauditory10abrainstem auditory10aevoked potential10aprimates10asomatosensory10avisual1 aDowman, R.1 aWolpaw, Jonathan1 aSeegal, R., F.1 aSatya-Murti, S.  uhttp://www.ncbi.nlm.nih.gov/pubmed/275170301987nas a2200205   4500008004100000022001400041245008200055210006900137260001200206300001200218490000600230520135500236653003701591100002401628700002201652700001901674700002001693700002101713856004701734       1984                        eng d  a0196-070900aPsychoacoustic and electrophysiologic effects of partial eighth nerve damage.0 aPsychoacoustic and electrophysiologic effects of partial eighth   c02/1984  a43–480 v53 aThe 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.10aVestibulocochlear Nerve Diseases1 aCacace, Anthony, T.1 aGoldstein, J., C.1 aParnes, S., M.1 aSatya-Murti, S.1 aWolpaw, Jonathan  uhttp://www.ncbi.nlm.nih.gov/pubmed/653419301136nas a2200193   4500008004100000022001400041245007700055210006900132260001200201300001400213490000700227520056400234653001100798100002000809700002100829700002400850700002100874856004700895       1983                        eng d  a0013-469400aLate auditory evoked potentials can occur without brain stem potentials.0 aLate auditory evoked potentials can occur without brain stem pot  c10/1983  a304–3080 v563 aThe 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.10aHumans1 aSatya-Murti, S.1 aWolpaw, Jonathan1 aCacace, Anthony, T.1 aSchaffer, C., A.  uhttp://www.ncbi.nlm.nih.gov/pubmed/6193943