Psychophysiotogy. 30 (1993), 347-358. Cambridge University Press. Printed in the USA.Copyright © 1993 Society for Psychophysiological Research

Lead stimulation effects on reflex blink, exogenousbrain potentials, and loudness judgments

WILLIAM M. PERLSTEIN, EVELYN FIORITO,ROBERT F. SIMONS, AND FRANCES K. GRAHAMDeparttiient of P.sychology, University of Delaware, Newark

AbstraetPrepulse inhibition of the reflex blink by a weak stimulus shortly preceding a blink-eliciting stimulus has beendescribed as a sensorimotor gating phenomenon that may protect processing of the first stimulus. To determinehow a .stitnulus configuration that elicits prepulse inhibition also affects exogenous evoked potentials and perceivedloudness of the paired stimuli, the three types of response were recorded simultaneously under four conditions;tone pairs of 75-110 dB and 75-75 dB and single control tones of each intensity. Two studies using differentintrapair intervals found that blinks and exogenous potentials peaking after 50 ms were smaller for the secondtone of pairs than for equal-intensity single tones. Pairing also reduced the loudness of 110-dB second tones, butthe loudness of 75-dB first and second tones was unaffected or increased. These effects are discussed in terms ofparallel processing of transient, untnodulated infortnation in specific paths, steady-state modulated informationin nonspecific paths, and a context-dependent effect on loudness judgments.

Descriptors: Prepulse inhibition. Startle, Blink reflex. Exogenous evoked potentials, Midlatency potentials.Magnitude estimation

Recent developtnents in psychophysiology suggest the existenceof a powerful sensoritnotor gating tnechanism by means ofwhich even weak stimuli autotnatically attenuate response toshortly following higher intensity stitnuli. One line of researchhas extensively studied this prestitnulus effect on the generalizedstartle reflex; a second line of research has investigated scalp-recorded event-related potentials (ERPs) and has found thatexogetious ERPs are also attenuated when a stimulus is repeatedat sitnilarly shott intervals. The present research, by employingboth prestimulus paradigms and simultaneously recorded refiexstartle blink and auditory ERPs, links the two t-e.search lines and,by obtaining judgments of stimulus loudness, links the hypoth-esized gating tnechanistn to concotnitant perceptual effects.

Prestimulus inhibition of startle is a robust phenomenondetnonstrated not only in hutnans but also in pigeons and vari-ous rodents (Anthony, 1985; Hoffman & Ison, 1980). Atiy briefchange in prestimulation —such as an onset, offset, or change

This research was supported hy Natiotial Institute of Mental Healthgrants K5-MH21762 and R01-MH42465. The work was reported in partat the Twenty-ninth Annual Meeting of the Society for Psychophysio-logical Research in New Orleans, LA. October 1989, and Expetitnent2 was subtiiitted by the first author in partial fulfillment of requirementsfor the Master of Arts degree.

We gratefully acknowledge the assistance of Richard Freed in theseoring of midlatency evoked potentials.

Address reprint requests to: France.s K. Grahatn or Robert F. Simons,Department of Psychology, University of Delaware, Newark, DE 19716.

in tone pitch —can be effective even near detection threshold,although effectiveness increases with intensity increase. Unlikerefractory effects, pair members —Stimulus I (SI) and Stimu-lus 2 (S2) —need not be in the same modality. Further, althoughrefractory effects are maximal within 1-2 ms, prestimulus in-hibition has a nonmonotonic temporal course that does notreach tnaxitnum for about 100 ms. The prestimulus effect is alsonot due to learning, to the middle ear refiex, or to peripheralresponse interaction (Grahatn & Murray, 1977; Hammond,McAdam, & Ison, 1972), but it does appear to depend on tran-sient characteristics ofthe prestimulus; an SI lasting no longerthan 6 ms is sufficient to produce an effect and a 20-ms SI pro-duces as great an effect as an SI sustained until S2 onset(Ciiardina, 1989; Graham & Murray, 1977). Although prepulseinhibition is tnediated at the midbrain level (Leitner & Cohen,1985; Leitner, Powers, Stitt, & Hoffman, 1981) and is undimin-ished during sleep (Silverstein, Graham, & Callaway, 1980), itis only weakly present in human infants (Graham, Strock, &Zeigler, 1981) and does not mature fully until near adolescence(Ornitz, Guthrie, Kaplan, Lane, & Norman, 1986).

The interest in prepulse inhibition arises from the assumptionthat it refiects a sensoritnotor gating mechanism with conse-quences for normal perception and, conversely, that dysfunc-tional gating leads to abnortnal perception. Graham (1975, 1979)suggested that the tnechanistn, nortnally initiated when transient-sensitive neural elements detect an SI onset or other change,tnight protect SI processing by inhibiting disruptive responsesto an S2. Without such a mechanism, temporally adjacent stim-

347

348 . Pertstein et al.

uii might more easily mask or merge with one another so thatonly a single stimulus could be perceived or two stimuli couldbe perceived but with altered characteristics. As Braff et al.(1978) noted, such dysfunction in an early protective mechanismmight account for schizophrenics' experience of stimulus "fiood-ing," in which irrelevant stimuli cannot be shut out and evenweak stimuli seem too intense. Their finding that a group ofmedicated schizophrenics had less blink inhibition than controlsprovides some support for this hypothe.sis. Simons and Giardina(1992) and Perlstein, Fiorito, Simons, and Graham (1989) ob-tained similar reductions of prepulse inhibition in a sample ofundergraduates identified by questionnaire as prone to percep-tual aberrations.

Prepulse inhibition of ERPs in normal controls and reducedinhibition in schizophrenics has also been reported (e.g., Adieret al., 1982). The ERP research employed pairs of equal-intensitystimuli, a variant ofthe blink paradigm, and measured the pos-itive (P) and negative (N) deflections P50/P1, NlOO/Nl, andP2OO/P2, which peak, respectively, at about 50, IOO, and 200 ms.Tbese and two earlier potentials —P30 and N40 —were measuredin the present research because any differential effects of pre-stimuli on early and later ERPs could be informative about therelation between refiex activity and brain activity. All five po-tentials are considered exogenous, that is, stimulus driven andrelatively obligatory. Like prepulse inhibition of blink, theseERPs are evoked by rapid, brief stimuli and are unchangedby stimulus durations exceeding about 30 ms (Onishi & Davis,1968), although a nonspecific component of Nl with slowerrecovery periods than specific Nl components (Naatanen &Picton, 1987) may continue to change for up to 90 ms (Putnam& Roth, 1990). Also, as in the prestimulus inhibition of blink,the pairing effect on one of these potentials (P50) is very latein maturing (Freedman, Adler, & Waldo, 1987). The functionalsimilarities suggest that prepulse effects on blink and ERP maybe related, but the two responses have not been studied simul-taneously or under identical conditions.

The evidence for diminished prepulse inhibition of startle andERPs in populations with perceptual problems is consistent withthe assumption that the paradigm has perceptual consequences.With one exception, however, these perceptual consequenceshave not been asses.sed. Cohen, Hoffman, and Stitt (1981) foundthat magnitude judgments of a strong glabellar tap preceded bya weaker tap, or by a weak tone, were reduced relative to judg-ments of the strong tap presented alone. An equally importantquestion for the sensory gating hypothesis is whether or not SIperception is also affected.

The present research included two experiments; an initialstudy with a 120-ms intrapair interval expected to yield maxi-mal inhibition and a second study with a 500-ms interval closeto the upper limit for obtaining inhibition. In Experiment 1,subjects judged the loudness of single control stimuli and thesecond stimuli of pairs; in Experiment 2, SI, S2, and singlestimuli were judged.'

Various stratagems were employed to circumvent the prob-lems involved in simultaneously recording blink and ERPs. Byusing only four conditions and longer intertrial intervals than

' The judgment task might have attentional effects on blink andERPs that would not be measurable with the pre.sent design. However,attention effects are relatively small compared with the prepulse effectand, when both SI and S2 are judged, tend to cancel one another(Balaban, Anthony, & Graham, 1985: Hackley & Graham. 1987).

custotnary in ERP re.search and more subjects and tnore trialsper condition thati customary in blink tesearch, we coniprotni.sedbetween the confiicting needs for many trials to resolve ERPsand few trials to avoid blink habituation. We also included weakand intense S2s to protect against the possibility that intensestimuli would provide too few ERPs uncontaminated by vol-ume-conducted tnyogenic potentials. Blink contamination wasfurther dealt with by correcting ERPs for their regression onblink and eye movement activity.

MethodSubjectsUndergraduate students (Experiment \:N=22;1 women, 15tnen; mean ± SD age 19.2 ± 1.3 years, range 18-23 years andExperiment 2; Ai' = 24; 11 women, 13 men; age 19.0 ± 1.2 years,range 18-23 years) were either paid subjects or received coursecredit in introductory psychology. They signed consent fortnsand satisfactorily completed a medical screening questionnaire.Eleven additional subjects were excluded for the following rea-sons; too few reflex blinks (n = 3), noisy electrode (n = 2),artifact in ERP recordings (n = 5), rating instructions misun-derstood (n = 1).

Stimuli and RecordingsStimuli were 80()-Hz sine waves at 75, 90, and 110 dB (A .scale),calibrated with a fiat-plate coupler attached to a General Ra-dio sound-level meter (1551-C). Stimuli were generated by Coul-bourn Signal (S81-86) and VCG Function Generators (SCi-1273)and gated (Coulbourn S84-()4, 100/ts ri.se/fall) through a Coul-bourn Audio-Mixer Amplifier (S82-24) for binaural delivery toTDH-49P earphones tnounted in a Tracor RA-125 headset.Coulbourn Universal Timers (S53-21) and one-shots, computertriggered, determined tone duration (40 ms) and onset-to-onsetintrapair intervals (Experiment 1,120 ms; Experiment 2, 500 ms).

Recording of blink activity was made via miniature elec-trodes (Silverstein & Graham, 1978) in a bipolar electromyogram(EMG) configuration. The electrodes, filled with Beckman elec-trode paste, had impedances below 5 kohms and were centered3 mm apart over the upper pretarsal portion of left m. orbicu-laris oculus. Full-wave rectification and integration by a Coul-bourn Contour-Following Integrator (S76-01; calibrated timeconstant 155 ms) followed amplification by a Princeton AppliedResearch 113 preamplifier (bandpass 10 Hz to 10 kHz; gain 5K).A bipolar electrooculogram (EOG) from sites centered 0.5 in.(1.27 cm) above and below the right eye and monopolar ERPleads from Irontal (Fz) and central (Cz) midline sites referredto the left mastoid and connected to a left earlobe ground wererecorded from miniature Med Associates electrodes (resistanceof < 10 and <5 kohms, respectively). Potentials were led throughCoulbourn Hi-Gain Bioamplifiers (S75-O1) with bandpass of0.1-40 Hz and gains 5K and 20K, respectively. The four chan-nels were sampled by a PDF'-l 1/34 cotnputer every 1.4 tns for973 ms, beginning 35 ms prior to onset of control stimuli or thefirst stimulus of a pair.

ProcedureSubjects were .seated in a reclining chair with headrest supportin a test chamber that comtnunicated via intercom with the ad-jacent control room. Each experiment included the satne fourconditions: two control conditions of a low (75 dB) and a high(110 dB) tone presented alone and two prepulse conditions inwhich the low-intensity tone preceded either the high-intensity

Blink, ERPs, perception 349

tone (low-high condition) or a low-intensity tone (low-low con-dition). Each condition occurred equally often in each of fourblocks of 20 trials, and subjects were randotnly assigned with-out replacement to begin at a different row of a 4 x 24 matrixformed by six 4 x 4 Latin squares. Intertrial intervals varied ran-domly between 18 and 28 s, except for a 3-tnin rest period thatfollowed trial 40.

After every trial, subjects performed an unspeeded, unsig-nalled magnitude estimation task (Cohen et al., 1981; Stevens,1956). To anchor judgtnents, two 90-dB tones were given priorto each block of trials and sttbjects were informed that thesewere standard tones assigned a loudness of 10. Other tones wereto be rated in relation to the standard so that, for exatnple, atone that seemed twice as loud as the standard should be rated20; a tone that seemed half as loud should be rated 5.

Subjects in Experiment 1 rated only the second stimulus ofeach pair and every stimulus presented alone. In Experiment 2,ratings were made according to four instructions (A-D), eachassigned to a different block with assigntnents approxitnatelycounterbalanced over subjects: Rate (A) any stimulus presentedalone and the first of a pair, or (B) singles and the second of apair, or (C) only paired stimuli, reported in the order first thensecond, or (D) only paired stimuli, reported in the order secondthen first. Table 1 shows the nutnber of ratings of each stimu-lus under each condition.

Data Reduction and Analysis

Reflex blink. Subjects were included in the final sample onlyif they had at least 70% acceptable nonzero blink responses inthe high-intensity single-totie condition. A Fortran program(Balaban, Losito, Simons, & Grahatn, 1986), using standardadult parameters for EMG with the time constant we employed,determined trial acceptability and measured peaks in the enve-lope of integrated EMG activity in a witidow 20-150 ms afteronset of control toties and the second of paired tones. A totalof 2.95% and 2.03% of trials were discarded by the progratnin Experiments 1 and 2, respectively, tiiainly because of base-line activity. Acceptable trials lacking a tneasurable responsewere a.ssigned a value of zero (Humphreys, 1943). Latencies arenot reported because titning circuits were separate for sitigle andpaired conditions and, thus, even small differences in timing

Table 1, Number of Loudness Ratings per Subjectof Low (L) and High (H) Tones

Tone"

LHLLLLLHLH

Total

Experitnent 1,instruction

B

2020

20

20

80

A

555

5

20

Experiment

B

55

5

5

20

2, instructions

C

5555

20

D

5555

20

Note: Tones were pre.sented alone or as members of low-low or low-high pairs. L = 75 dB; H = 110 dB. Instructions were A: rate all singletoties and first tone of all pairs: B: rate all singles and second of all pairs;C: rate pairs only, first tone first; D: rate paits only, second tone first." Underscored letters indicate tones rated for loudnes.s.

would bias condition comparisons. As noted by Hackley andGraham (1987, Experiment 2), prepulse effects on latency aresmall and vary nonmonotonically with intrapair interval so thatit is, in any case, difficult to make secure predictions about pair-ing effects on latency.

For statistical analyses, the individually scored trials wereaveraged per subject per condition to yield measures of proba-bility (ratio of acceptable nonzero trials to total acceptable tri-als), peak magnitude (includes zero trials), and peak amplitude(excludes zero trials). The size measures were subtracted frombaseline, and each of the three measures was analyzed by 2 x 2within-subject analyses of variance (ANOVAs) for Pairing (sin-gle vs. S2) X Intensity (low vs. high). Planned contrasts were alsomade between responses to each S2 and its same-intensity sin-gle control.

ERP deflections. Single-trial ERPs were corrected for ver-tical EOG (Gratton, Coles, & Donchin, 1983; Miller, Gratton,& Yee, 1989) and averaged per subject for each condition at eachelectrode site, ln a recent symposium, participants from six lab-oratories discussed the results of correcting a common data setusing their own correction methods (Brunia, Mocks, & van denBerg-Lenssen, 1989). There was general agreement that correc-tion itnproves data quality and that the six methods yield quitesitnilar ERPs. We selected the Gratton et al. method, which hasbeen cross-validated by the authors and by OToole and Iacono(1987), because it estimates artifact correction factors separatelyfor eye movements and blinks and because these propagationfactors are computed on the residual ERP/blink activity afterstimulus-locked activity has been removed. Therefore, the es-timates of the degree to which blink artifacts are present at theEEG electrodes (i.e., the blink propagation factors) should notbe itifiated due to the coincidence between stimulus-related blinkand (genuine) ERP activity. So, when the correction procedureis applied, it should remove only that aspect ofthe ERP that isattributable to blink artifact.

Based on the assumption that respotise in paired conditionsequals the response to SI alone plus the response to S2, paired-condition ERPs were further adjusted by subtracting from themthe corrected ERP evoked by the low-intensity control stimu-lus. Low-intensity control and prestimuli evoked nearly identi-cal activity during the S1-S2 interval, but a slow negativity,persisting beyond the interval in both the corrected low-alonecontrol and the two paired conditions, drove the S2-evoked re-sponse above 0 V (Figure 1). The subtraction procedure largelyremoved this effect. Any remaining deviations from zero wereremoved by aligning control and S2 waveforms so that their firstpoststimulus points were set to zero.

Examination of the individual-subject corrected waveformsrevealed that ERPs of five subjects in Experiment 1 had sharp33-78-^V artifacts in the midlatency region, possibly associatedwith a head jerk induced by high tonic muscle tension. Thesedeflections resulted in bimodal distributions of peak amplitudesfor P30 (high and low-high conditions) and N40 (high con-dition), and means of the five subjects exceeded by factorsof 6, 7, and 11, respectively, comparable peaks in ERPs of theremaining subjects. Data from the five subjects- were thereforediscarded.

^ The five subjects were included in a preliminary report given atthe meetings of the Society for Psychophysiological Research (Perlstein,Fiorito, Simons, & Graham, 1989).

350 IV. M. Pertstein ct at.

120 ms-40

Low-High

Low-Low

Low

200 400 600 800Time (ms)

Figure 1. Mean ERP waveforms at Cz for low-alone and paired stim-uli before subtraction of the low-alone waveform from the pairedwaveforms. (ERP corrected for vertical EOG: on.set-to-onset intervalsbetween paired stimuli 120 ms and 500 ms.)

The effects of pairing, intensity, and site on ERP amplitudeand factor scores were evaluated by 2 x 2 x 2 within-subjectANOVAs and planned contrasts between S2s and .same-intensitycontrols. As with blink, latencies are not reported but, to avoidextracting a spurious factor from principal components analy-sis (PCA), the first major peak (P30) in individual-subject ERPsfor high-intensity S2s was aligned to the P30 peak in the high-intensity control ERP; a subject's ERP for low-intensity stimuliwas then adjusted by the same amount. Adju.stments averaged— 1.9 ± 3.8 (SD) ms in Experiment I and —3.3 ± 5.2 ms inExperiment 2.

Each of the major defiections was evaluated separately. ForN1(X) and P200, ba.se-to-peak amplitudes were computer scoredfrom the individual-subject average ERPs by an algorithm thatdetermined, for each condition and site, the least positive devi-ation from baseline within the window 80-160 ms and the leastnegative deviation between the NlOO peak and 240 ms. The algo-rithm was unsuitable for identifying midlatency potentials be-cause, with the narrow windows required, false peaks were toooften identified at window extremes, that is, on a rising or fall-ing slope rather than an infiection point. Consequently, the ma-jor measure of these potentials consi.sted of the factors extracted,for each experiment separately, from a varimax-rotated PCA

derived from the covarianee matrix. The PCA was perfortnedon the first 85 ms using BMDP (P4M) softwatx.

A supplementary measure of the midlatency potentials, suit-able only for ERPs of the high-intensity stimuli, was obtainedby hand .scoring base-to-peak amplitudes from data sheets listingsampled voltages in the first 85 ms of per-subject per-conditionERPs. Two individuals following written rules and examplesagreed on the scoring of all but three records; these cases wereresolved by a third scorer. Briefly, the rules defined a peak asthe most positive (negative) point that was also a point of in-fiection between positive-going and negative-going changeswithin windows of 15-40ms, 30-60 ms, and 45-85 tns, for P30,N40, and P50, respectively. Such a point had to meet the crite-ria that (a) at least two successive slope changes of the same signoccurred on both sides of the peak; (b) a minitnum defiectionof 0.48 ^V occurred by, at most, 4.2 ms on either side of theidentified peak point; (c) at least 4.2 ms separated consecutivepeaks; and (d) the time between component onset-inflection andoffset-inflection points was at least 8.4 m.s. Peaks could not beidentified in 20 instances, distributed approximately equallyamong electrodes, conditions, and cotnponents. Nineteen to 21subjects in Experiment 1 and 18-24 subjects in Experiment 2who had one or more identifiable peaks in both paired and con-trol conditions and at both electrode sites remained for statis-tical analysis.

Magnitude estimation. In Experiment 1, the 20 ratings ofeach S2 and of each control stimulus (Table 1), averaged to yieldfour means per subject, were analyzed for the effects of pair-ing and intensity and for planned contrasts between each S2intensity and its intensity control.

In Experiment 2, averaging of the ratings per stimulus perinstruction yielded 16 means (Table 1); 12 tneans for the fourpaired stimuli and four means for the two control stimuli. Be-cau.se preliminary analyses showed that instructions did notaffect ratings of paired stimuli, these ratings were collapsedacross instructions. However, ratings of control stimuli wereaffected by instructions (/•"[1,231 = 8.64, p < .01). They wetehigher under B than under A instructions and interacted withintensity (F\ 1,23] = 7.19, p < .025), tefiecting greater effectson rating high- than low-intensity control stimuli, presumablydue to the context in which stimuli were rated; under A instruc-tions, only 25% of rated stimuli were high intensity, but underB, 50% were high intensity. Because of the.se differences, for-ward effects of SI on S2 were analyzed, as in Experitnent 1,usitig the control ratings obtained under B; backward effects ofS2s on SI, analyzed separately, u.sed control ratings obtainedunder instruction A.

Results

Reflex BlinkThe goal of assessing ERP and perceptual concotnitatits of theprepulse inhibition paradigm requires that the paratneters em-ployed produce blink inhibition. This condition was met al bothintrapair intervals, with inhibition generally gteater at the tnax-imally effective 120-ms interval. Blink tnagnitude, atnplitude,and probability were significantly reduced as a function of pair-ing, not only for the standard paradigtn of low-followed byhigh-intensity stitnuli but also for the low-low conditions, withthe exception of amplitude in Experitnent 1 (Tables 2 and 3).ANOVAs also revealed significant Pairing x Intensity inter-

Blink, ERPs, perception 351

Table 2. Mean Blink Magnitude, Amplitude, andProbability Associated With Low and High Tones

Table 3. E Ratios frotn Analyses of Reflex Blink VarianceDue to Pairing and to Intensity

Condition

Experiment 1: 120 msLow-highHigh aloneLow-lowLow alonen

Experiment 2: 500 msLow-highHigh aloneLow-lowLow alonen

Magnitude(,,,V)

7.969.0

1.920.322

53.883.3

3.819.824

Atnplitude(/<V)

28.687.025.435.09

70.893.514.932.817

Probability

.353

.973

.063

.62922

.828

.962

.168

.56024

Source

Experiment 1: 120 ms •Pairing (P)"

HighLow

Intensity (1)''P X Idf

Experimcnl 2: 5(X1 msPairing (P)

HighLow

Iniensitv (I)P X Idf

Magnitude

47.4**66.3**IS 2**76.5**75.9**1,21

33.4**26.3**19.8**30.4**6.0*1,23

Ainplitude(f<V)

17.7**17.7**3.3

26.6**13.2**

1,8

18.0**19.1**12.1**17.2**

1.61, 16

Probabili

141.1**116.3**68.9**64.4**<11. 21

85.0**7.6*

54.5**155.3**

9.4**1, 23

Note: Magnitude = mean of all trials; amplitude = mean of nonzerotrials.

actions for blink magnitude at botb intervals and for blink prob-ability at the 500-tns interval; that is, high-intensity S2s weretnore reduced by pairing than were low- intensity S2s. This in-teraction, which contradicts findings that inhibitory effects ofa given SI are independent of S2 intensity (Hoffman & Lson,1980), was likely due to floor effects and was reduced or elimi-nated when blink amplitude, which excludes zero-magnitude re-sponses, was analyzed.

Evoked PotentialA question of pritnary interest is whether lead stimulation af-fects early and later ERPs differently. Figure 2, which illustratesERP wavefortns at Cz. suggests that the atnplitudes of poten-tials, beginning with F50, were reduced under paired conditions

Note: Magnitude = mean of all trials; amplitude = mean of nonzerotrials."Second metiibers of pairs versus single .same-intensity stimuli. 'M 10 dBversus 75 dB.*p < .05. '*p < .01.

and that, like the prestimulus inhibitory effect on blink, reduc-tions were greater with the shorter intrapair interval. In contrast.N40 was generally more negative for S2s than for single stim-uli and F30. although sensitive to the intensity difference, wasrelatively unchanged by lead stimulation in botb experiments.

Statistical analyses of base-to-peak amplitudes confirmedthe illu.strated pairing effects on NlOO and F200 (Table 4); siteeffects reflect the larger amplitudes and greater inhibition at Czthan at Fz (Table 5). Intensity effects, significant at botb sites,were also greater at Cz. For F200 in Experiment 1 only, inhibi-tion was greater witb high than with low S2s but the three-way

120 ms 500 ms

-40High

100 200 300 400Time (ms)

100 200 300 400Time (ms)

Figure 2. Mean ERP waveforms at Czfor high-alone stitnuli compared withhigh siimulus 2 (S2) in the low-high pair(lop) and for low -alone stimuli comparedwith low S2 in the low -low pair (bottom)al 120-ms and 500-ms intervals. Begin-ning wilh a positive deflection at about25 ms, five deflections are apparent inthe ERPs to high-intensity stimuli: P30.N40, P50, NlOO. P200.

352 W.M. Peristein et al.

Table 4. E Ratios from Analyses of ERP VarianceDue to Pairing, Electrode Site, and Intensity

120 ms

Experiment I: 120ms Experiment 2: 500 ms

Source NlOO F200 NlOO P200

Pairing (P)"Site (S)*Intensity (I)'P X SP X IS X IP X S X Idf

110.1**16.9**23.3**6.0*

<112.8**

I.I1, 21

51.2**49.2**11.7**25.8**5.4*

<14.6*

1. 21

25.5**56.3**56.5**26.4**

<l33.7**

1.11.23

6.0*131.8*"23.9*'32.7*«

1.110.0*'

1.51,23

"Second members of pairs versus single same-intensity stimuli. *Fz ver-sus Cz. ' 110 dB versus 75 dB.*p< .05. •*p< .01.

interaction indicated that the greater inhibition with high S2occurred mainly at Fz.

PCA scores constituted the primary measure of midlatencycomponents. Factor loadings from the first 4 of 10 factors areplotted in Figure 3. These loadings were nearly identical for thetwo studies and accounted for 91 % and 93% of the variance inthe two data sets. Their maximum loadings suggest identifica-tion of Factors 4, 2, 3. and 1 with P30. N40. P50. and the ris-ing slope of NlOO. respectively. Comparison ofthe mean factor.scores at Cz (Table 6) with the expanded midlatency potentialsat Cz (Figure 4) indicates that the pattern of pair and single stim-ulus differences in factor scores corresponds well to the patternapparent in the respective potentials.

Results of ANOVAs and planned contrasts on midlatencyfactor scores (Tables 6 and 7) showed that the P50 reductionsassociated with pairing were significant for both high- and low-intensity pairs with the 120-ms intrapair interval but only for thehigh-intensity pair with a 500-ms interval and only at Cz in botbexperiments. There was some evidence that an effect of lead

Table 5. Mean NlOO and P200 Amplitudes (n V)Under Pair and Single Conditions

Condition

Experiment 1: l 2 0 m s ( »High

VzCz

LowFzCz

Experiment 2: 500 ms (nHigh

FzCz

LowFzCz

= 22)

= 24)

Pair

-8 .6-18.3

-6 .5- 9 . 7

-15.8-28.1

-7 .8-11.7

NlOO

Single

-20.4**-38.3**

-20.7**-29.7**

-24.8-44.0**

-16.9**-29.2**

Pair

4.27.8

2.83.7

13.826.7

6.914.2

P200

Single

23.8**34.4**

14.0**28.7**

13.235.5*

8.427.2**

.4 0

*p < .05 for pair - single differences, "p < .01 for pair - single dif-ferences.

20 40 60Time (ms)

Figure 3. Factor loadings for midlatency ERP components from Ex-periments 1 (top) and 2 (bottom). Factors 1, 2. 3, and 4 correspond, re-spectively, to NlOO Onset Slope. N40. P50. and P30.

stimulation began as early as the N40 potential, but unlike NlOO,pairing led to significant enhancement in the 120-ms study, thatis. greater rather than lesser negativity (Figure 4. Table 6). Siteeffects and interactions al.so differed from those of NlOO. Inboth experiments, N40 was larger at Fz than at Cz and was larg-est for high-intensity stimuli; in the 500-ms study, nonsignifi-cant pairing effects were opposite in direction as a function ofsite. The earlier F30, although significantly larger for high- thanfor low-intensity stimuli, was not significantly affected by pre-stimulation for either paired-stimulus intensity at either intra-pair interval.

Supplementary analyses of midlatency base-to-peak ampli-tudes, scorable only for high-intensity conditions (.see Methodsection), were in general agreement with results obtained for fac-tor scores. Frestimulation significantly reduced F50 amplitudein both experiments (pairing F | 1,20] = 13.7; F[I,I7] = 13.2;p < .01) and at both Cz and Fz(p< .01). Pairing also increasedN40 significantly in the Cz lead for the 120-ms group (F[ 1,19] =4.95, p < .05). Amplitudes of P30 potentials were unaffected bypairing at eitber intrapair interval.

Magnitude EstimationsThe perceptual concomitants of stimulus pairitig were evaluatedseparately for forward effects of lead stimulation on the phe-nomenal magnitude of S2 and for backward effects of S2 on SI(Figure 5).

Blink, ERPs, perception

Table 6. Mean Factor Scores for Midlatency ERPs Under Pair and Single Conditions

353

Condition

Experiment 1: 120 ms (n = 22)High

FzCz

LowFzCz

Experiment 2: 500 ms (n = 24)High

FzCz

LowFzCz

Pair

.287

.436

- .478- .508

.429

.460

- .356- .366

P30

Single

.451

.560

- .432-.337

.308

.431

-.435- .471

Pair

- .517- .260

.102- .040

- .479-.1.10

.345

.328

N40

Single

- .397.128

.421

.564**

- .752- .010

.261

.438

Pair

- .167-.033

- .403- .529

- .480- .070

- .206- .074

P50"

Single

.124

.946**

-.191.253**

.045

.872**

-.251.164

*p < .01 for pair - single differences.

Forward effects on judgments of the high-intensity stitnuluswere in agreement with the prestimulus inhibition effect and thefindings of Cohen et al. (1981); that is, judgtnents were lower(less loud) when the high S2 was preceded by a weak prestimu-lus than when the high-intensity stimulus was unpaired. How-ever, when S2 atid SI were the same low-intensity stimuli, S2was judged to be slightly louder than its low-intensity control.These observations were supported in both Experitnents 1 and2 by statistically significant interactions of Pairing x Intensity(respectively, F[l,21 ] = 9.51; F[ 1,23] = 22.70; p < .01), by sig-nificant reductions in tbe loudness ratings of high-intensity S2s(respectively. Fl 1.21 ] = 6.57. p < .05; F[ 1.23] = 20.13. p < .01).and by significantly enhanced loudness of the low-intensity S2(F[l,21] = 22.04. p <.001 ;F[ 1,23] = 5.77. p < .05).

Only Experitnent 2 provided data for evaluating backwardeffects. SI ratings under both paired conditions were enhanced

relative to ratings of the low-intensity control stimulus (Figure 5.left); the extent of enhancement was a function of S2 intensity,that is. high S2s were associated with greater enhancement ofSI than were low S2s. Although the main effect of conditions(two pairs and control under A instructions) was significant(F[2.22] = 4.43. t = .78. p < .05 with Greenhouse and Geisser[1959] correction), planned comparisons revealed significantSI enhancement only for the low-high pair (F[1.23] = 8.19.p < .01). For the low-low pair. F(1.23) = 2.71. p = .13.

Discussion

Blink and ERPsFrestimuli did have inhibitory effects on both reflex blink andERPs. confirming a similarity suggested by previous researchin which the responses were studied separately under different

1 0

-5

0

5

10

10

-5

0

5

10

120 ms

High-S2

500 ms

High-

L0W-S2

Low

20 40 60 80Time (ms)

20 40 60Time (ms)

Figure 4. First 85 ms of ERP wave-, forms shown in Figure 2. with the scale

8 0 s^Panded to illustrate changes in the mid-latency ERPs P30. N40. and P50 as alunction of stimulus pairing and intensity.

354

Table 7. F Ratios for Analyses of Midlatency ERP EactorScores Due to Pairing, Electrode Site, and Intensity

"Second members of pairs versus single same-intensity stimuli. ''Fz ver-sus Cz. 'UOdB versus 75 dB.*/7< .05. **p< .01.

stimulus conditions and by different investigators. Our findingsfurther suggest that ERPs were not contaminated by volumeconduction of potentials associated with blink and eye move-ments. We employed a correction method (Gratton et al.. 1983)that adjusted for artifactual activity without removing commonstimulus-related activity. Because too few subjects had sufficienttrials in the same condition, both with and without blinks, wecould not directly compare associated ERPs, but several aspectsof our data are reassuring: tbe corrected waveforms are consis-tent with those expected from auditory stimuli; both low-highand low-low pairs showed statistically significant prepulse in-hibition; inhibition was greater at the shorter intrapair interval;and ERPs were not more positive at frontal sites, as would beexpected if lid and eye movement artifact had not been elimi-nated. The smaller frontal than central response also arguesagainst artifactual potentials contributed by unmonitored facialmuscles. This argument may not apply to confounding ERPswitb the postauricular refiex. but if that refiex had an effect, theeffect should have peaked between 9 and 30 ms and should haveshown prepulse inhibition (Hackley. Woldorff. & Hillyard.1987). Thus, if the corrected P30 in our studies was substantiallyinfiuenced by the postauricular reflex, pairing would have re-duced it. but it did not.

ERP amplitudes were several times larger in the pre.sent stud-ies than in traditional studies, whose rapid delivery rates (<levery 3 s). many more trials, and lower intensity stimuli yieldmean values that rarely exceed 10/iV for Nl or 1-3 ^V for mid-latency potentials. However, the few .studies using interstimu-lus intervals of 8 s or longer and stimuli of 75 dB or higher havefound control-stimulus amplitudes more nearly comparable tothose in the present experiments: Adler et al. (1982) reportedF50. NlOO. and F200 means of 8.9. 22. and 28 ^V. respectively,to clicks (peak intensity 1 10 dB. mean intensity 75 dB); Roth.Dorato, and Kopell (1984) reported 11.8. 28. and 28/xV for thesame peaks for 110-dB 50-ms noisebursts; and Putnam and Roth(1990) reported about 25-30 /iV for NlOO (the higher valueresulted from excluding trials with probable blink artifact)and 29 /tV for P200 for the first 15 presentations of 105-dB30-ms noise.

Backward

W.M. Peristein et al.

Forward

Source

Experiment 1: 120 ms (df = ],2\)Pairing (P)"Site (S)"Intensity (1)'P X SP X IS X I

Experiment 2: 500 ms (df = 1, 23)Pairing (P)Site (S)Intensity (1)P X SP X 1S X 1

P30

< l3.5

15.2**

^ !

2.9

<1<115.6**

< 1<1

3.7

N40

5.6*5.2*7.4*3.2

9.7**

<l10.0**12.9**6.4*

<115.1**

P50

6.9*5.2*9.1**9.2**

6.6*

5.2*15.8**

1.84.6*5.8*

11.7**

(0O>

(0OC(0

oc

o

33

30

27

120-ms

500-ms

LH• 21.6

33.0

•28 .9*

23.8

S1 ControlStimulus Rated

S2

Figure 5. Mean loudness ratings as a function of stimulus conditionsin experiments with 120-ms and 5(H)-ms intrapair intervals. Ratings ofsingle control slimuli are plotted on Ihc ccnler verlical (high alone abovethe cut: low alone below) with backward modulations (SI ratings) andforward modulations (S2 ralings) plollcd lo ihc loll and righl. icspcc-livcly. H = high. L = low; underscored Ictlcrs indicate which stimulusof low-low or low-high pairs was rated. */; < .05 and **p < .025 lorsingle - pair diflercnces.

Nature of Prepulse Inhibition

Late exogenous ERPs. The significant reductions in NlOOand P200 amplitude, associated with S2s in the present studies,are consistent with inhibitory effects observed in ERP sttidiesusing paired auditory stimuli under relatively similar conditions(Adler et al.. 1982; Freedman et al.. 1987; Kathmann & Engel,1990), as well as in "recovery-cycle" paradigms where intrapairintervals are varied to estitnate the time for recovery of S2 re-spon.se to SI levels (e.g., Butler, 1973; Davis. Mast. Yosliie. &Zerlin. 1966). Several other ERP studies have shown that ERFresponse to S2. like the inhibitory effect on blink, is also re-duced by crossmodal pairing (Davis. Osterhammel. Wier, &Gjerdingen, 1972) and by the off.set of a sustained prestimulus(Butler, 1973; Hillyard & Ficton, 1978).

Debates have focused on whether or not these short-tertrtrepetition effects are due to ititrinsic and/or extrinsic inhibition.Intrinsic tnechanisms, such as bomosynaptic deprcssioti andmembrane desensiti/ation. result in reduced respotisiveness. orrefractoriness, by decreasing the efficacy of the direct pathwaythat mediates a response; in contrast, extrinsic mechanisms are"active" processes that are tnediated by a parallel pathway ex-ternal to. but synapsing with, the direct path (Davis & File.1984). Although either mechanism could be operative in thepresent studies, itihibition by a crosstnodal prepulse would itn-ply the participation of an extrinsic path. As Naatanen and Pic-ton (1987) pointed out. the nonspecific component of Nl is

Blink, ERPs, perception 355

especially susceptible to crossmodal inhibitory effects. Bloch(1972) reported that weak visual prestimuli. delivered 200 tnsprior to an auditory second stimulus, reduced both the N1-P2vertex ERP and the simultaneously recorded blink.

Blink. Although the physiological mechanistn of short-termreductions in the late exogenous potentials is uncertain, thereis considerable evidence from studies of rat. tnouse. and cat thatprepulse inhibition of reflex startle is a form of extrinsic in-hibition. P50 inhibition may also depend on extrinsic inhibition.For auditory whole-body startle in the rat. the direct path liessolely within the hindbrain. It receives inputs via the ventralcochlear nucleus, branches from the main sensory projection inthe paralemniscal zone, synapses in the ventral nucleus retic-ularis pontis caudalis. and the signal thence goes to effectors(Davis. Gendelman. Tischlcr. & Gendelman. 1982; Leitner,Powers. & Hoffman. 1980). Electrical stitnulation of these ar-eas elicits startle; bilateral lesions of the areas abolish or atten-uate it.

Frepulse inhibition is produced by a tnore rostral extrinsicpath in the midbrain that has an unknown number of synapsesbut. for auditory prestitnuli. probably includes at least the ex-ternal subdivision of inferior colliculi. polysensory lateral teg-tnentutn. and. specifically, the cuneiform nucleus before feedingback to the direct path. The external nuclei of inferior colliculidiffer frotn the central nucleus in functional characteristics byhaving less sensitivity to rapid stitnulus ri.se time, less abilityto follow fast repetition rates, and longer latencies (Willott &Deniuth. 1986). Lesions of these subdivisions also have differ-ent effects. Those including only the central nucleus leave star-tle unaffected, but lesions including external nuclei facilitatethe acoustic startle refiex (Parham & Willott. 1990) and atten-uate or abolish inhibition by auditory but not by visual prestitn-uli (Leitner & Cohen. 1985). suggesting that visual prestimuliaccess the indirect path via some other route. Lesions later inthe path, in tegtnentutn, abolish inhibition by both auditory andvisual prestitnuli (Leitner et al.. 1981). Thus, the extrinsic pathcannot initiate startle but maintains a tonic inhibitory effect anda phasic inhibitory modulation of startle by prestitnuli.

Differential effects on P30 and P50. The finding that pair-itig did not affect P30 but did reduce P50 and later ERPs is con-sistent with the idea that P30 and P50 ate not generated byneural elements in a serial path. The differential effect cannotbe ascribed to insensitivity in measuring a relatively small po-tential. In response to single stitnuli. Pa/P30 defiections wereas large as those of Pb/P5()/Pl and did vary significantly withstitnulus intensity. Further, the differential effect was found inboth experitnents and also by Freedman et al. (1987). who didnot report P30 data but did note that F30 was not reduced atthe 500-ms interval that produced P50 decrement.

The differential pairing effect on P30 and P50 is consistentwith other functional diffetences between these ERFs. Erwinand Buchwald (1987) found a very fast recovery rate for P30.with responses stable even at rates up to 10/s. In contrast. P50was markedly decreased or absent at the faster rates. A sitni-lar pattern was found in the cat equivalent' of these potentials

' Although Buchwald. Hintnan. Norman. Huang, and Brown (1981)lentalivcly associated cat wave 7 with human vertex Po and cat wave Awith human Pa/P30. the identifications were revised as a result of theirlater studies so that cat wave7 was equated with Pa/P30 and cat wave Awith Pa/P50/Pl.

(Buchwald. Hinman, Norman. Huang. & Brown, 1981; Hin-man & Buchwald. 1983). The two potentials also differed inboth species as a function of sleep state and general anesthesia-inducing agents, with P50 again more sensitive.

There is al.so evidence that P30 and P50 arise from differentanatomical pathways., Buchwald et al. (1981) reported loss ofP30 following bilateral aspiration of auditory cortex, whereasP50 survived even hemispherectomy that involved massive de-generation in the medial geniculate. part ofthe specific projec-tion system through the thalamus. The authors suggested thatthe two potentials are "generated differentially through fore-brain systems which receive auditory information in parallelfrom the brain stem, rather than serially from the primary thal-atno-cortical pathway through association cortex relays" (p. 92).In further work. Hinman and Buchwald (1983) recorded fieldand single-unit potentials to trace the subcortical system forP50 frotn the midbrain tegmentum. including the nucleus cune-ilormis. to the midline intralaminar thalamus. Like prepulseinhibition of blink. F50 was facilitated by total removal of theinferior eolliculus. whereas stimulation of only its central nu-cleus elicited the very short latency responses typical of F30rather than F50. Human studies mapping the scalp distributionof ERFs (e.g.. Cacace. Satya-Murti. & Wolpaw. 1990; Scherg& Von Cramon. 1986). as well as intracranial recordings (Cele-sia. 1976; Velasco & Velasco. 1986) and studies of patients withtemporal lobe lesions (e.g.. Kileny. Faccioretti. & Wilson. 1987;Woods, Clayworth. Knight. Simpson. & Naeser. 1987). are gen-erally consistent with the assumption that F30. but not F50.reflects activity in primary auditory cortex.

Summary. The prestimulus effects on blink and F50 appearto be transmitted by an extrinsic path through a nonspecificpolysensory reticular formation that includes some nuclei com-mon to the two responses. However, at least for startle, theinhibitory effect arises prior to convergence of modalities be-cause inhibition by an auditory prestimulus can be blocked with-out blocking a visual prestimulus effect. The fact that F30 isunaffected by prestitnuli suggests tbat inhibition does not feedback to the specific sensory pathway from which it derives. Inthe case of startle, inhibition may be transmitted either to inter-neurons or to motor cells in the direct startle path. In the caseof F50. the reduced activity is apparently transmitted to anauditory-specific cortical area adjacent to the primary area.Thus, the cortical areas involved in early sensoriperceptual pro-cessing appear to receive in parallel at least two kinds of stimu-lus infortnation: information that is independent of a precedingstitnulus and information that is not.

Loudness Versus Blink and ERPLoudness ratings did not show changes completely concordantwith the changes in blink and ERFs. Although low-intensitySis redticed the loudness of high-intensity S2s. in keeping withtheir reducing effect on blinks and on ERFs beginning with F50.low-intensity Sis significantly increa.sed the loudness of low-intensity S2s. despite reducing S2 blinks. Further, the loudnessof paired low-intensity Sis was also increased, whereas ERFsfor SI were apparently unaffected (Figure 1). Thus, the jointfindings of significant loudness increases for a low-intensity S2and for a low-intensity SI (in the low-high pair) clearly disso-ciate perceptual changes from changes in blink and ERFs.

The absence of any reduction in SI loudness is compatiblewith a hypothesized tnechanism protecting its processing from

356 W.M. Peristein et al.

interruption (Graham. 1975). but the fact that low S2s were alsojudged louder suggests the need for some other or additionalmechanism. Dissociations between ERPs and loudness estimateshave been consistently demonstrated in single-stimulus para-digms: NI-F2 magnitude grows more slowly with intensity thandoes loudness and saturates at intensity levels at which loudnessis still increasing, which led Davis and Zerlin (1966) to concludethat the generators of these potentials did not lie on the directpath to psychological .sensation but on a parallel path. A dis-sociation might also be predicted for at least those exogenousERFs that are sensitive mainly to onsets and that recover rap-idly. Because loudness depends on steady-state portions of astimulus envelope (Gerken. Bhat. & Hutchison-Clutter. 1990).it presumably requires a neural mechanism with longer recov-ery periods capable of maintaining a more lasting representa-tion of a stimulus. Auditory areas of cortex do receive .separateinformation from both types of processors.

Although separate sampling of processors with different fil-tering properties probably cannot explain directionally oppositechanges in loudness compared with blink and ERFs. interactionsbetween transient and sustained neural paths might do so. Breit-meyer and Ganz (1976) suggested that such interactions couldaccount for nonmonotonic backward effects of pairing on visualpercepts. These effects were always more or less inhibitory, neverenhancing perception above that provided by single stimuli, butthe interactions could, under assumptions of nonlinear effectsat different processing levels, produce enhancement as well asinhibition, depending on the spatiotemporal patterns.

Another type of explanation is suggested by the nature of theperceptual effects themselves, considered without reference toblink and ERF changes. Fairing appeared to produce loudnessassimilation, at least in the standard prepulse inhibition low-high pair. That is. loudness of pair members shifted toward oneanother and. relative to their respective control values, did sosymmetrically-SI increa.sed 10.87% and S2 decreased 10.18%,a nonsignificant unsigned difference. Such shifts have often beenascribed to central tendeney. adaptation level, or context effectsin that the shift is toward some weighted average of the set ofstimuli. Context apparently also influenced ratings of our con-trol stimuli. When the rating set included two high- and two low-intensity stimuli, control stimuli were rated louder than whenthe set contained only one high-intensity stimulus.

Other studies, using a variety of paradigms and methods ofmeasuring loudness. lend support to the idea that context plays

an important role in loudness perception (Cowan. 1987; Eltna-sian & Galambos. 1975; Elmasian, Galambos, & Bernheim.1980; Irwin&Zwislocki, 1971; Feak. 1940; Zwislocki. Ketkar,Cannon. & Nodar. 1974; Zwislocki & Sokolich. 1974). WhenS1-S2 intensity differences were large (10-50 dB), findings forboth forward and backward modulating effects of low-highpairs agree with ours and show, in addition, the satne centraltendency effect with a high-low pair; that is, both forward andbackward loudness judgments show reduction in loudness ofhigh intensities and enhancement of low intensities. When inten-sities were equal or the difference was small (2-4 dB), findingsacross studies differed in direction or showed no effect.

If context affects loudness and other sensory judgments, bywhat mechanism are such effects achieved? Two recent studiesconcluded that context effects do not result from biases imposedat a respon.se selection stage but. rather, affect the loudness rep-resentation itself (Algom & Marks, 1990; Schneider & Parker.1990). However, it isunclear whether the effect occurs at an earlysensory stage or at a later cognitive or judgment stage (Coats& Dickey. 1972; Cowan, 1987; Elmasian & Galambos, 1975).

,'iummaryThe goal of the pre.sent studies was to determine perceptual con-sequences of a prepulse inhibition paradigm that, in previouslyunrelated studies, has revealed a powerful gating mechanism bywhich blink refiex and exogenous ERP responses to a stimulusare attenuated by a shortly preceding stimulus. By measuringboth types of response simultaneously, we found that both blinksand ERPs beginning with P50 were attenuated and that higherneural levels also received unattenuated infortnation transmittedon a different path and reflected in P30. We also found per-ceptual consequences of the paradigm but they appeared to becontext effects dependent on weighting the set of intensitiesrather than a gating effect dependent on the temporal order ofstimuli. A survey of the perception literature suggested that theapparent context effect of intensity was probably not due toour specific set of stimuli, but an orthogonal design balancingintensity for forward and backward modulations could deter-mine whether intensity or order is more effective and whetheror not they interact. More important, the finding that some con-text-dependent assimilation occurs in subjects with presumablynormal function ofthe hypothesized gating mechanistn makesit imperative to study perceptual as well as psychophysiologi-cal con.sequences in subjects with gating dysfunction.

REFERENCES

Adler, L. E., Pachtman. E., Franks, R. D., Pecevich. M., Waldo.M. C , & Freedman, R. (1982). Neurophysioiogical evidence for adefect in neuronal mechanisms involved in sensory gating in schizo-phrenia. Biological Psychiatry, 17, 639-654.

Algom, D., & Marks. L. E. (1990). Range and regression, loudnessscales, and loudness processing: Toward a context-bound psycho-physics. Journat of Experimentat Psychology: Human Perceptionand Performance, 16, 106-121.

Anthony. B. J. (1985). In the blink of an eye: Implications of reflex mod-ification for information processing. In P. K. Ackles. J. R. Jennings,& M. G. H. Coles (Eds.). Advances in p.sychophysiology (Vol. 1.pp. 167-218). Greenwich. CT: JAI Press.

Balaban, M. T.. Anthony. B. J.. & Graham, F. K. (1985). Modality-repetition and attentional effects on rellex blinking in infants andadults. Infant Behavior and Development, 8, 443-457.

Balaban, M. T.. Losito, B.. Simons. R. F., & Graham, F. K. (1986).Off-line latency and amplitude scoring of the human reflex eyeblink with Fortran IV. Psychophysiology, 23, 612 [Abstract).

Bloch, R. M. (1972). Inhibition and facilitation effects of a prepulse onthe human blink response to a startle pulse. Unpublished doctoraldissertation. University of Wisconsin, Madison.

Braff, D. L.. Stone. C , Callaway. E., Geyer, M.. Glick. I.. & Bali. L.(1978). Prestimulus effects on human starlle reflex in nortnals andschizophrenics. P.sychophysiology, 15, 339-343.

Breitmeyer, B. t i . , & Ganz, L. (1976). Implications of sustained andtransient channels for theories of visual pattern masking, saccadicsuppression, and information processing. P.sychological Review, 83,1-36.

Brunia. C. H. M., Mocks. .1.. & van den Berg-Lenssen, M. M. C. (1989).Correcting ocular artifacts in the EEG: A comparison of severalmethods. Journal of Psychophysiology, 3, 1-50.

Buchwald. J. S.. Hinman. C , Norman, R. J., Huang, C. M., & Brown.K. A. (1981). Middle- and long-latency audiiory evoked responsesrecorded from Ihe vertex of normal and chronically lesioned cats.Brain Re.search, 2(55. 91-109.

Butler. R. A. (1973). The cumulative effects of different stimulus rep-

Blink, ERPs, perception 357

ctition rales on the auditory evoked response in man. Electroenceph-alography and Clinical Neurophysiology, 35, 337-345.

Cacace, A. f., Satya-Murti, S., & Wolpaw. J. R. (1990). Human mid-dle-latency auditory evoked potentials: Vertex and temporal com-ponents. Electroencephalographv and Clinical Neurophysiology, 77,6-18.

Celesia, G. G. (1976). Organization of auditory cortical areas in man.Brain, 99, 403-414.

Coats, A. C , & Dickey, J. R. (1972). Postmasking recovery of humanclick action potentials and click loudncss. Journal ofthe .'\coiisti-cal Societv of America, 52, 1607-1611.

Cohen, M. E., Hoffman, H. S., & Stitl. C. L. (1981). Sen.sory magni-lude estimation in the conlexl of reflex modification. Journal ofExperitnental Psycholog v: Hutnan Perception and Perfonnatxce, 7,1363-1370.

Cowan, N. (1987). Auditory sen.sory storage in relation to the growthof sensation and acoustic informalion extraction. Journal of Exper-itnental Psvchologv: Hutnan Perception and Performance, 13,204-215.

Davis, H., Mast. T., Yoshie, N.. & Zerlin, S. (1966). The slow responseof Ihe human corlex lo audiiory slimuli: Recovery process. Electro-eticcphalography atid Clinical Neurophysiology, 21, 105-113.

Davis, H., Osterhammel. P. A.. Wier, C. C . & Gjerdingen, D. B. (1972).Slow vertex potentials: Interactions among auditoty. tactile, electric,and visual stimuli. Electroencephalography and Clinical Neurophys-iology, 33, 537-545.

Davis, H., & Zerlin, S. (1966). Acoustic relations of the human vertexpotential. Journal ofthe Acoustical Society ofAtnerica, 39, 109-116.

Davis, M., & File. S. E. (1984). Intrinsic and extrinsic mechanisms ofhabitualion and .scnsilization: Implications tor the design and anal-ysis of experiments. In H. V. S. Peek & L. Petrinovich (Eds.), Ha-hituation, .sensitization, and behavior (pp. 287-323). New York:Academic Press.

Davis. M., Gendelman. D. S.. Tischler, M. D., & Gendelman. P. M.(1982). A primary acoustic startle circuit: Lesion and stimulationstudies. The Journal of Neuroscience, 2, 791-805.

Elmasian, R., & Galambos. R. (1975). Loudness enhancement: Mon-aural, binaural, and dichotic. Journal of the Acoustical Society ofAmerica, 58, 229-234.

Elmasian, R., Galambos, R., & Bernheim. A. (1980). Lotidne.ss enhance-ment and decrement in four paradigms. Journal of the Acoustical.Society ofAtnerica, 67, 601-607.

Erwin. R.. & Buchwald, J. S. (1987). Midlatency auditory evoked re-sponses in Ihe human and Ihe cat model. In R. Johnson, J. W. Rohr-baugh, & R. Parasuraman (Eds.), Current trends in event-relatedpotential re.search (pp. 461-467). Amsterdam: Elsevier.

Freedman, R., Adler, L. E., & Waldo, M. (1987). Gating of the audi-tory evoked polenlial in children and adults. P.sychophysiology, 24,223-227.

Gerken. G. M., Bhal. V. K. H., & Hutchi.son-Clutter, M. (1990). Au-ditory lemporal integration and the power lunction tnodel. Journalof the Acoustical Society of Atnerica, 88, 767-778.

Giardina, B. D. (1989). Short and long tittie proce.s.sing in tnediatingprepulse inhibition ofthe startle blink reflex. Unpublished doctoralthesis. University of Delaware, Newark.

Graham. F. K. (1975). The more or less startling effects of weak pre-slimulalion. Psychophysiology, 12, 238-248.

Graham, F. K. (1979). Distinguishing among orienting, defense, andstartle reflexes. In H. D. Kimmel, E. H. van Olst, & J. F. Orlebeke(Eds.). The orienting reflex in hutnans. An international cotiferencespoti.sored by the Scientific Affairs Division ofthe North AtlanticTreatv Organization (pp. 137-167). Hillsdale, NJ: Eribaum.

Graham. F. K.. & Murray, G. M. (1977). Di.scordant effects of weakpresliniulation on magnitude and latency of Ihe blink reflex. Phys-iological Psvchologv, 5, 108-114.

Graham, F. K., Strock, B. D.. & Zeigler. B. L. (1981). Excitatory andinhibitory influences on reflex responsiveness. In W. A. Collins (Ed.).Aspects ofthe developtnent of cotnpetetice. Minnesota symposia onchildpsvchology (Vo\. 14, pp. 1-38). Hillsdale, NJ: Eribaum.

Gratton, G., Coles, M. G. H., & Donchin, E. (1983). A new methodfor off-line removal of ocular artifact. Electroetwephalography atidClinical Neurophysiology, 55, 468-484.

Greenhouse. S. W.. & Geisser. S. (1959). On methods in the analysis ofprofile data. Psychotnetrika, 24, 95-112.

Hackley, S. A., & Graham, I K. (1987). Effects of attending .selectivelyto the spatial position of reflex-eliciling and reflex-modulation stim-

uli. Journal of Experitnental Psychology: Human Perception andPerfortnance, 13, 411-424.

Hackley, S. A.. Woldorff, M., & Hillyard. S. A. (1987). Combined useof microreflcxcs and event-related brain potentials as measures ofaudiiory selective attention. Psychophv.siology, 24, 632-647.

Hammond! G. R., McAdam, D. W., & Ison, J. R. (1972). Effects ofprestimulalion on the elecnomyographic response associated withthe acoustic startle refaction in rats. Physiology and Behavior, 8,535-537.

Hillyard, S. A.. & Picton. T. W. (1978). On and off components in theauditor\' evoked potential. Perception and Psychophysics, 24,391-398.

Hinman. C. L.. & Buchwald. J. S. (1983). Depth evoked potential andsingle unit correlates of vertex midlatency auditory evoked responses.Brain Re.search, 264, 57-67.

Hoffman, H. S.. & Lson. J. R. (1980). Reflex modification in Ihe do-main of starlle. I. Some empirical findings and their implications forhow Ihe nervotis system processes sensory input. Psychological Re-view, 87, 175-189.

Humphreys. L. G. (1943). Measures of strength of conditioned eyelidresponses. The Journal of General Psychology, 29, 101-111.

lrwin. R. J.,& Zwislocki. J. J. (1971). Loudness effects in pairs of tonebursts. Perception and Psychophy.sics, 10, 189-192.

Kathmann, N., & Engcl, R. R. (1990). Sensory gating in normals andschizophrenics: A failure lo find strong P50 suppression in normals.Biological Psychiatry, 27, 1216-1226.

Kileny, P., Paccioretii. D., & Wilson. A. F. (1987). Effects of conicallesions on middle-latency audiiory evoked responses (MLR). Elec-troencephalography and Clinical .Neurophysiology, 66, 108-120.

Lcilncr. D. S.. & Cohen. M. E. (1985). Role of the inferior eolliculusin the inhibition of acoustic startle in the ral. Physiolog\' and Behav-ior, 34, 65-70.

Leitner. D. S., Powers. A. S., & Hoffman, H. S. (1980). The neuralsystem for the inhibition of startle. Bulletin of the PsychonomicSocietv, 14, 410-412.

Leitner. D. S.. Powers. A. S., Stitt. C. L.. & Hoffman, H. S. (1981).Midbrain reticular formation involvement in the inhibition of acous-tic startle. Physiology and Behavior, 26, 259-268.

Miller, G. A., Gratton. G.. & Yee. C. M. (1989). Generalized implemen-tation of an eye movement correction procedure. Psvchophvsiology,25, 241-243.

Niiaianen, R., & Picton, T. (1987). The Nl wave of the human electricand magnetic response to sound: A review and an analysis of thecomponent structure. Psychophysiolog_v, 24, 375-425.

Onishi. S., & Davis. H. (1968). Effects of duration and rise time of tonebursts on evoked V potentials. Journal of the Acoustical Society ofAtnerica, 44, 582-591.

Ornitz, E. M.. Guthrie. D., Kaplan. .A. R., Lane, J., & Norman. R. J.(1986). Maturation of startle modulation. Psychophysiology, 23,624-634.

OToole. D. M., & laeono, W. G. (1987). An evaluation of different tech-niques for removing eye-blink artifact from visual evoked responserecordings. Psvchophvsiologv, 24, 487-497.

Parham, K.. & Willott. .1. F. (1990). Effects of inferior eolliculus le-sions on the acoustic startle response. Behavioral Neuroscience, 104,831-840.

Peak. H. (1940). Time order error in successive judgments and in re-Ilexes. 11. As a function of the first stimulus of a pair. Journal ofE.\peritnental Psychology, 26, 103-115.

Peristein, W. M., Fiorito, E., Simons. R. F.. & Graham. F. K. (1989).Prestimulation effects on reflex blink and EPs in normal and schizo-typal subjects. Psychophysiology, .?6(Suppl.). S48.

Putnam, L. E.,& Roth. W.T. (1990). Effects of stimulus repetition, du-ration, and rise time on startle blink and automatically elicited P300.P.sychophy.siology, 27, 275-297.

Roth, W. T., Dorato, K. H.. & Kopell, B. S. (1984). Intensity and taskeffects on evoked physiological responses to noise bursts. Psvcho-physiology, 21, 466-481.

Scherg. M.. & Von Cramon. D. (1986). Evoked dipole source r>otentialsof the human auditory cortex. Electroetwephalography and Clini-cal Neurophysiology, 65, 344-360.

Schneider, B., & Parker. S. (1990). Does stimulus context affect loud-ness or only loudness judgments? Perception atid Psvchophvsics, 4S,409-418.

Silverstein. L. D.. & Graham, F. K. (1978). Eyeblink EMG: A minia-ture eyelid electrode for recording from orbicularis oculi. Psvcho-physiology, 15, 377-379.

358 W.M, Peristein et al.

Silverstein, L. D., Graham. F. K., & Callaway. J. M. (1980). Precon-ditioning and excitability of the human orbicularis oculi reflex as afunction of state. Electroencephalography and Clinical Neurophys-iology, 48, 406-417.

Simons. R. F.. & Giardina. B. D. (1992). Reflex modification in psy-chosis-prone young adults. Psychophysiology, 29, 8-16.

Stevens. S. S. (1956). The direct estimation of sensory magnitudes-loudness. American Journal of Psychology, 69, 1-25.

Velasco, M.. & Velasco, F. (1986). Subcortical correlates of the somatic,auditory and visual vertex activities. II. Referential EEG responses.Electroencephatography and Clinical Neurophysiology, 63, 62-67.

Willott. J. F..& Demuth. R. M. (1986). The influence of stimulus rep-etition on the acoustic startle response and on responses of inferioreolliculus neurons of mice. Brain Research, 386, 105-112.

Woods. D. L.. Clayworth. C. C , Knight, R. T.. Simpson. G. V., &Naeser. M. A. (1987). Generators of middle- and long-latency au-ditory evoked potentials: Implications from studies of patients withbitcmporal lesions. Electroencephalography and Clinical Neurophys-iology, 68, 132-148.

Zwislocki, J. J., Ketkar, L, Cannon, M. W., & Nodar, R. H. (1974).Loudness enhancement and summation in pairs or short soundbursts. Perception and Psychophysics, 16, 91-95.

Zwisloeki, J. J., & Sokolich, W. G. (1974). On loudne.ss enhancementof a tone burst by a preceding tone burst. Perception and Psycho-physics, 16, 87-90.

(RECEtvED January 31, 1991; ACCEPTED June 16. 1992)