02319nas a2200205   4500008004100000022001400041245010200055210006900157260001200226300001300238490000700251520166900258653003101927653002901958653002701987653001402014100002102028700001802049856004602067       1978                        eng d  a0013-958000aAcute and chronic antiepileptic drug effect on the T complex interhemispheric latency difference.0 aAcute and chronic antiepileptic drug effect on the T complex int  c02/1978  a99–1070 v193 aAntiepileptic drugs may significantly affect brain function in the absence of overt toxicity or excessive serum drug levels. A clinically practical monitor of such effects would be of considerable value in clinical research and practice.

Auditory evoked responses were recorded from patients before and after initiation of antiepileptic drug therapy and from patients on therapy for at least 1 year. T complexes were isolated (Wolpaw and Penry, 1975), and Ta peak ipsilateral versus contralateral latency differences were determined.

In 13 patients beginning phenobarbital, more than half the postdrug determinations were significantly increased over the patients' predrug control values in the first 30 days and thereafter, and grossly abnormal values were frequent. In 10 patients beginning phenytoin, latency differences were similarly increased, although grossly abnormal values were less common. In 2 patients beginning clonazepam, 14 of 15 postdrug determinations were significantly increased, and five were grossly abnormal. In no patients were serum drug levels above the therapeutic ranges. In 40 patients chronically treated with phenobarbital or primidone, phenytoin, or a combination of phenytoin and phenobarbital or primidone, abnormal latency differences were obtained in 33, 36, and 29% of the determinations, respectively.

The Ta peak ipsilateral versus contralateral latency difference is an internally controlled correlate of higher level specific sensory function which is sensitive to acute and chronic therapy with phenobarbital, phenytoin, or clonazepam in therapeutic dosages. With further investigation, it may be of clinical use.10aAntiepileptic drug effects10aAuditory evoked response10aHemispheric difference10aT complex1 aWolpaw, Jonathan1 aPenry, J., K.  uhttp://www.ncbi.nlm.nih.gov/pubmed/62427201639nas a2200169   4500008004100000022001400041245007900055210006900134260001200203300001400215490000700229520113600236653001301372100002101385700001801406856004501424       1978                        eng d  a0013-469400aEffects of ethanol, caffeine, and placebo on the auditory evoked response.0 aEffects of ethanol caffeine and placebo on the auditory evoked r  c05/1978  a568–5740 v443 aA previous paper (Wolpaw and Penry 1975) described separation of the 75-250 msec portion of the AER into N1P2, a product of large areas of cortex, and the T complex, probably a product of secondary auditory cortex. With monaural stimulation, the T complex is larger and earlier on the side contralateral to stimulation and on the right side. Thirty-one normal adults received 3 oz. of ethanol, 300 mg of caffeine, or placebo. Monaural AERs were recorded before intake in all cases, 1 and 4 h after ethanol and 80 min after caffeine or placebo. Blood levels of ethanol and caffeine were measured. Placebo produced mild (20%) decreases in N1P2 amplitude. Caffeine did not decrease N1P2 amplitude. It did produce a statistically significant 2% decrease in Ta peak latency. Ethanol reduced N1P2 amplitude markedly at 1 h and mildly at 4 h. Placebo did not affect hemispheric differences. Caffeine significantly increased the Ta peak ipsilateral vs. contralateral latency difference in 3 of 7 individuals. Ethanol significantly increased it in 3 of 6 subjects at 1 h and in 7 of 10 at 4 h, primarily by increasing ipsilateral latencies.10aPlacebos1 aWolpaw, Jonathan1 aPenry, J., K.  uhttp://www.ncbi.nlm.nih.gov/pubmed/7776301828nas a2200169   4500008004100000022001400041245006100055210006000116260001200176300001300188490000700201520134800208653001801556100002101574700001801595856004501613       1977                        eng d  a0013-469400aHemispheric differences in the auditory evoked response.0 aHemispheric differences in the auditory evoked response  c07/1977  a99–1020 v433 aThe separation of the 80-250 msec portion of the AER to click stimulation into N1P2, produced by large areas of cortex, and the T complex, probably produced by secondary auditory cortex, was recently described (Wolpaw and Penry 1975). The present study investigated the ipsilateral vs. contralateral and right vs. left hemispheric differences in N1P2 and T complex latencies and amplitudes. One msec clicks at 60 dB above threshold were presented at 4.7 sec intervals monaurally to 32 normal adults and binaurally to 13 of the 32. AERs were recorded from vertex and temporal referred to a balanced non-cephalic reference electrode. For monaural stimulation, N1P2 and T complex amplitudes were significantly greater and T complex latency was significantly less over the contralateral and right hemispheres. The ipsilateral vs. contralateral and right vs. left hemispheric amplitude differences were significanlty greater for the T complex than for N1P2. Binaural results, which provided in additional measure of right vs. left hemispheric differences, were in agreement with the monaural findings. The results are consistent with neurophysiologic and behavioral findings in regard to ipsilateral vs. contralateral and right vs. left hemispheric differences and support the hypothesis that the T complex is produced by secondary auditory cortex.10aReaction Time1 aWolpaw, Jonathan1 aPenry, J., K.  uhttp://www.ncbi.nlm.nih.gov/pubmed/6887802233nas a2200169   4500008004100000022001400041245005800055210005500113260001200168300001400180490000700194520176100201653001701962100002101979700001802000856004502018       1975                        eng d  a0013-469400aA temporal component of the auditory evoked response.0 atemporal component of the auditory evoked response  c12/1975  a609–6200 v393 aWe 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.10aTime Factors1 aWolpaw, Jonathan1 aPenry, J., K.  uhttp://www.ncbi.nlm.nih.gov/pubmed/53139