Newborn heart-rate response and response habituation as a function of stimulus duration

JOURNAL

OF EXPERIMENTAL

Newborn

CHILD

PSYCHOLOGY

6, 265278

Heart-Rate Response and as a Function of Stimulus

(1968)

Response Habituation Duration1

RACHEL K. CLIFTON University of Iowa AND FRANCES K. GRAHAM University

AND HELEN of Wisconsin

M. HATTON

The heart-rate response of newborns to auditory stimulation was found to be an inverted U-function of stimulus duration. Groups of 20 Ss each were tested with a 2, 6, 10, 18, or 30-second 75 db stimulus. Response to all stimuli was a heart-rate acceleration whose peak magnitude, latency, and duration varied with stimulus duration and with stimulus repetition. Maximal response occurred following the lo-second stimulus. Repetition of the four longest stimuli led to response decrement but there was no habituation of response to the a-second stimulus. It was suggested that conflicting results of earlier studies might be reconciled on the assumption that the duration yielding maximal response is a function of stimulus intensity.

It is a well-established finding that increasing stimulus durations up to 100 or 200 milliseconds increases the magnitude of various psychophysical and neurophysiological responses, but duration effects beyond this range have received little attention. It is possible that excitatory effects might occur over a wider range with certain types of response and that inhibitory effects might develop if durations were sufficiently prolonged. Autonomic responses, for example, might be particularly likely to show effects of prolonging stimulation since they are capable not only of brief, “phasic” changes but of sustained, “tonic” responses thought to be related to general activation level (Malmo, 1959). Several studies have, in fact, reported duration effects on heart rate (HR) and on the GSR, but results have been conflicting. Heart-rate ‘This research was supported by grants HD01490 and K3-MH-21762 from the National Institutes of Health and by a postdoctoral Public Health Fellowship to Rachel K. Clifton. Computer services were provided through grant FRO0249 to the Biomedical Computing Division and an NSF grant through the University of Wisconsin Research Committee. The authors wish to express appreciation to W. Keith Berg and Rebecca Gerlach for assistance in many phases of this work. 265

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respon%s, with which the present paper is concerned, were unrelated to shock durations from 0.1 t’o 15.0 seconds in a study by Wegner and Zeaman (1958) but were an inverted U-function of shock duration from 0.1 to 10.0 seconds in a study by Church, LoLordo, Ovcrmier, Solomon, and Turner (1966). With auditory stimuli (Black, 1964; Keen, Chase and Graham, 1965) and with a nitrogen stream which indented the skin (Steinschneider, Lipton, and Richmond, 1965), HR increased monotonically with durations from 1.0-10.5, 2.0-10.0, and 1.0-5.0 seconds, respectively. Since these studies differed in the organism investigated, in the stimulus used, in the intensity of stimulation, and in the measure of response, there are many possible explanations of the discrepant findings. However, differences in stimulus intensity and in response measurement seem the most probable candidates. Both in psychophysical work, as reflected in the reciprocity law relating intensity and time, and in the Church et al. (1966) study, the peak of excitatory duration effects has been found to occur earlier with more intense stimuli. Thus, the discrepancy between the monotonically increasing function found in three studies and the inverted U-function obtained by Church et al. (1966) might be due to the relatively greater intensity of even a weak shock stimulus compared to an air-stream or to moderately intense auditory stimuli. If so, an inverted U-function might also be found if longer durations of the latter stimuli were used. This was tested in the present study. Wegner and Zeaman’s failure to find any relation between shock duration and HR response may be explained by their method of measuring HR response-the peak-to-valley difference occurring in the ten beats following shock onset. Heart-rate responses frequently show waves of response which may vary in the latency of onset, steepness of rise to a peak, the slope of decline, and the total duration of displacement, as well as in the direction of change. Unless characteristics of the full response are known, indices can radically distort the picture, as Graham and Clifton (1966) have noted. If, for example, shock elicits the common diphasic response of acceleration followed by below baseline deceleration and if proIonging a stimulus elicits a more proIonged response, a peak-tovalley measure limited to a ten-beat period might be based on the full response following a short stimulus and only a portion of the accelerative phase following a long stimulus. Black (1964) also used an index of response which is difficult to interpret-the greatest difference between HR in a 3-second prestimulus period and HR in any 3-seconds of a 20second poststimulus period. He found not only that response magnitude increased with stimulus duration but that latency also increased. He

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suggested that the latency change meant either that HR response occurred to the offset of the stimulus or that the response was temporarily suppressed in the longer duration groups by continuing stimulation. Since latency referred to the time from stimulus onset to the point of peak change, another possibility is that larger responses took longer to reach a peak. To avoid these problems of interpreting response indices, second-bysecond curves of HR change were obtained in the present study which is a more detailed analysis and extension of the Keen et al. (1965) experiment. In addition to the original 2- and lo-second stimuli, durations of 6, 18, and 30 seconds were employed. Two questions were of major concern: whether or not the duration-response function would be an inverted U, and whether this function would vary with repeated stimulations. If response decrement occurs with repeated stimulation and if this habituation varies with stimulus duration, response could not be the same function of duration on late as on early trials and an average over all trials might mask a changing relation. For example, if there were slower habituation of response to .longer stimulus durations, a positive relation between duration and response would develop even when there was no relation initially. This positive relation would be produced by the persistence of response to the longer stimuli after responses to shorter stimuli had disappeared. Similarly, more rapid habituation of response to longer stimulus durations could, depending on the initial relation, attenuate a positive relation, abolish it, or even produce an inverted U. METHOD

Subjects All infants who were born in University Hospitals, Madison, Wisconsin during the course of the original Keen et al. (1965) study or during the present extension were selected as Ss if they met predetermined criteria of normality. The normality criteria were: (a) birth weight greater than 5 pounds or diagnosis of full-term status; (b) normal spontaneous or low-forceps delivery; (c) and Apgar rating of general condition at birth of seven or higher (Apgar, 1953). Of the infants selected, 12 were replaced because parents refused permission, 19 because of apparatus or procedural error, and 14 because crying, regurgitation, or movement led to illegible records. One hundred infants completed the experiment. They were divided equally among five stimulus-duration groups balanced for sex. The 2second and lo-second groups each consisted of both control and experimental Ss from the Keen et al. (1965) experiment. Control Ss were 24-

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hours older than experimental Ss but since responses on the first sessions of testing were .shown not to differ significantly, these data were pooled. Data for t,he 6-, 18-, and 30-second groups were obtained subsequently. Within the 2-10 study and within three consecutive steps in gathering the extension data, 8s were randomly assigned to stimulusduration groups. The three steps were (a) ten Ss each in the 6- and 18second groups, (b) ten Ss in the 30-second group, and (c) ten Ss each in the *6-, 18-, and30-second groups. Mean age of Ss was, in order of increasing stimulus duration, 54.9, 46.5, 55.6, 44.7, and 43.8 hours. Bpparatus

and Procedure

Except for difference in stimulus duration, the general procedure was the same’ for all Xs. An infant was transported to the laboratory in a mobile closed crib which also served as the testing unit. Sessions began within 2 liours after feeding. An S was placed in a supine position, EKG electrodes and respiration strain gauge were attached, and S was swaddled to reduce movement. A pacifier was offered if the infant became irritable. Continuous polygraph recording of EKG and respiration began 2 minutes before the first stimulus and continued until 2 minutes after the fifteenth stimulation. Interstimulus intervals, 90 seconds from offset of one stimulus to onset of the next, and the stimulus durations were controlled electronically and were also recorded on the polygraph. The stimulus was qualitatively a rough-sounding buzz produced by recording the rectangular output of a pulse generator set at 300 pps with on-off time approximately one to nine. Intensity of the stimulus was 75 db re 0.0002 microbars as measured by a General Radio Type1551-C Sound-Level meter placed at the site of the S’s head. Background sound level was approximately 43 db with equipment operating. There were several, presumably minor, differences between procedures for the first 60 and the last 40 Ss. The first 8s were tested in a quiet basement laboratory but not in the IAC sound-attenuated room available for later Xs. In both circumstances, the testing room was air-conditioned and maintained at a temperature between 76 and 78’F. There was, at the same time, a change in polygraphs, from Gilson to Offner, and a change in EKG electrodes from Welsh suction electrodes to Beckman Biopotential electrodes. Respiration recording was also omitted for the last 40 Ss since efforts to find a relation between HR and respiration proved unsuccessful (Chase, 1965). These procedural differences may account for a lower prestimulus level in the later-tested Ss. However, the response of later-tested Xs, matched for stimulus duration and adjusted for prestimulus level, did not differ in any of the characteristics which proved to be significant in the overall analyses.

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HR Measurement For each S on each trial, the average length of a cardiac cycle was determined during the first prestimulus second and during each of 20 seconds following stimulus onset (poststimulus seconds). All cardiac cycles (R-R intervals) in a given second contributed to the average, including fractions of a cycle. In averaging, cycle lengths were weighted in proportion to the fraction of the second which they occupied. Average cardiac cycle length was then transformed to average HR in beats per minute (bpm) for each second. For statistical analyses and graphing, data were averaged into three-trial blocks. In the rare instances of partially illegible records, data were interpolated if only a few cardiac cycles were missing. If data for a full trial were illegible, the average of the other two trials in the same trial block was substituted. A record was considered too illegible to retain in the study if it could not be read for 10 seconds following any of the first three trials, on any two consecutive trials, or on more than three trials altogether. RESULTS

Prestimulus-Poststimulus

Relation

Prestimulus levels in the five groups are shown in Table 1. They are the means of HR during the first second preceding each of the 15 trials. Although there were no significant differences either among Duration groups (F = 1.76 df 4,95, error MS = 621.8) or across trial blocks (F = TABLE 1 MEANS AND REGRESSION COEFFICIENTS (BETA) OF POSTSTIMULUS ON PRERTIMULTJS HR FOR EACH STIMULUS GROIJP

PRESTIMULUS

Stimulus group

6 10

123.2 126.2 125.6

18

117.S

2

All

Prestimulus mean

30 groups

123.9 123.4

Pooled beta

Range among

of betas seconds

--.13 --.21 -.32 --.I7 -.17 - .IS

-.07 -.03 -.09 -.04to

to --.22 to --.32 to -.37 -.26

-.Ol

to

-.27

-

0.69, dj 4,380, error MS = 55.6), change scores for each second were adjusted for variation in prestimulus levels. Since HR change following stimulation is a function of HR level preceding stimulation (Lacey, 1956; Benjamin, 1963)) removing this source of variability reduces the variance in response measures.

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CLIFTOK,

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AND

HATTON

Adjustment utilized the pooled iinear regrca,?ion c:oefic:cbnt, after tckts indicated that t,he assumptions of linearity and homogeneity could be reasonably well satisfied. Linearity was tested on each poststimulus second of each Duration group. Of the 100 t&s, there was significant curvilinearity on only 7 seconds, scattered among groups and seconds. Homogeneity of l&ar regression was also tested at each poststimulus second across trial blocks of each group as well as across the five groups. The regression coefficients within groups ranged from --.Ol to -.37 (Table 1) ; these values are in the range usually reported both for adult and newborn Ss. Although regressions were heterogeneous within the 6-second group (F = 2.51; df 99,180O; p < .Ol), they were homogeneous within the other groups and among groups (overall F = 0.37; df 4,90). Steinschneider et al. (1965) also found that regression coefficients did not change as a function of stimulus duration. The exact regression equation used to adjust scores for each second was AD=D-bbox (X-s), w h ere AD = Adjusted Difference, D = Poststimulus HR - Prestimulus HR, bDI = -.18, and 2 = 123.4, the overall prestimulus mean. A Peak-Magnitude score was also used in one analysis, b,, = -.26, for this score. Response

Curves

The response to all stimulus durations was a wave of acceleration beginning within l-2 seconds of stimulus onset and reaching a peak between 3 and 6 seconds. This response appears to be typical of the newborn and has been reported for a variety of stimulus conditions (e.g., Bartoshuk, 1962; Bridger and Reiser, 1959; Davis, Crowell, and Chun, 1965; Graham, Clifton, and Hatton, 1968; Lipton, Steinschneider, and Richmond, 1961). It is illustrated in Fig. 1 for the first trial block, i.e., for the average of the first three trials. Adjusted score values are plotted at the midpoint of the interval which they represent. Several additional features can also be observed from the curves in Fig. 1. Response following the a-second stimulus was smaller than following any of the longer stimuli. Not only was peak magnitude less but it was reached earlier and the total durat,ion of the accelerative wave was shorter. Responses to the other stimuli varied among themselves but differences are not striking. It is interesting that slopes during the rising phase were roughly parallel for all stimuli although, again, the 2-second curve showed a less steep rise. The declining phase of the response appeared to be more gradual than the rise and to be more variable both within and across groups. Following the longest stimulus, but no other, there was a substantial decline below prestimulus level in the final seconds. This greater decline in response to Ihe 30-second stimulus

NEWBORN

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RESPONSE

could also be observed on curves, not shown, of the first trial alone. However, on no second of the first trial were there significant differences among groups, or in linear or quadratic trends across groups, during the time a stimulus was actually present. That is, there was no difference among all five duration groups on the first 2 seconds, among the four longer Duratons on seconds 3-6, among the three longest Durations on seconds 7-10, or between 1% and 30-second Durations on seconds 11-20. Anovas yielded F’s ranging from 0.21 to 2.14 on these 20 tests. 10.00 8.75 7.50 o B ti z P k k 0

6.25 5.00 3.75 2.50 ‘1.25

~5 ?5

45

6.5

6.5 10.5 SECONDS

12.5

145

16.5

18.5

1. HR response on trial block 1 with stimulus durations of seconds (N = 20 per stimulus duration group).

FIG. 30

2.5

20.5

2, 6, 10, 18, and

Response on the last trial block is illustrated in Fig. 2. Except for a secondary phase of deceleration falling below prestimulus levels in t,he 30-second curve, the response to all stimuli still appears to be a wave of acccleL,ation whose onset begins within a second or two of stimulus onset. The response is reduced, however, both in peak magnitude and in duration. Reduction is especially pronounced in the 6- and 30-second groups. While these groups differed only slight,ly from the lo- and 1% second groups on the first trial block, on the final trial block they showed less acceleration than the 2-second group. To determine whether or not these complex fluctuations in HR represented reliable changes following stimulus onset, HR during each poststimulus second was compared with HR during the second that preceded stimulation. Table 2 lists the seconds, for each group and each trial block, on which p values of the t-ratio were less than .05 (twotailed probability). Except for responses to the 30-second stimulus during

272

CLIFTON,

GRAHAN,

AND

HATTON

a-f5 t 150i!50r

,,”

6.25

~~~~

L3 ;i a

-p5-125-

.HC’

i

2.50 -

..

2 See

-__-.-

.._ ‘_

I6082 1esec 30 Set

‘..

3 “5,7.11 75 +.5

1 2.5

I 4.5

1 65

. . .I *i

‘.

1 6.5

1 10.5

I 12.5

‘,(_..

I 14.5

. . ..

. ..

I

I

16.5

16.5

I 20.5

SECONDS

FIG. 2. HR response on trial block 5 with stimulus 30 seconds (N = 20 per stimulus duration group).

durations

of 2, 6, 10, 18, and

seconds 17-20, all significant changes were increases in HR. The trends are similar to those illustrated by Figs. 1 and 2. Heart-rate increase following the 2-second stimulus was significant for only a few seconds and there was little change across trial blocks. In contrast,, there was a reliable response to the longer stimuli for 9-15 seconds on the initial trial block and the number of seconds of reliable change decreased irregularly across trial blocks. The reliability of successive, second to second, changes was also analyzed. Except on the last trial block with the 30-second stimulus, there was always a reliable increase in HR between the first and second POSTSTIMEI,US

SECONDS FROM

TABLE 2 SHOWING SIGNIFICANT PRESTIMULUS LEVEL* Trial

Stimulus duration 2-Second increases B-Second increases IO-Second increases l&Second increases 30-Second increases 11/30-Second decreases *p

< .05.

1 14 3-17 2214 l-15 2-10 20

2

2-6 2-11 2-5 3-8 228 0

HR

CHANGE

blocks 3

l-5 2-10 2-13 2-11 2-5 17-18

4

2-5 2-7 227, Y-7 24 0

5

11

2-5 0 l-7 2-5 0 18-20

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poststimulus seconds and, with one other exception, between the second and third seconds. Further significant increases were relatively rare but were more frequent on the first trial block. These findings indicate, first, that there is no change in the latency of onset of acceleration as a function of repeated stimulation. They also suggest, as do the figures, that prolonging stimulation does not elicit continuing acceleration of HR but serves, rather, to slow the return to baseline. Significant second to second decreases were also found but they did not exhibit any clear pattern. Stimulus

Duration

and Repetition

Efects

While the preceding section suggested that there were differences in response as a function of stimulus duration and repetition, the, significance of these effects was not tested directly. To make such tests with data of manageable size, two general types of analysis were employed. The first used the full 20 seconds of poststimulus data divided into four successive 5-second periods. Variance due to seconds, to the five duration effects, and to trial blocks 1 and 5 were analyzed separately for each period. The second type of analysis used all five trial blocks but analyzed the variance due to trial blocks and duration separately for each of three indices of response: Peak Magnitude, Peak Latency, and Response Duration.2 This method of analysis permitted the use of trend tests across seconds, in the first case, and across trial blocks in the second case. The sources of variance which proved significant in one or more analyses are shown, with their error terms, in Tables 3 and 4. A question of major interest was whether or not response would be an inverted U-function of stimulus duration. Although the overall main effect of Duration was significant only for Peak Latency, the quadratic component of trend was significant in four of the analyses and, as Fig. 3 and 4 illustrate, the shape of the curves was an inverted U-function of the log of Duration for all three indices and all but the last five seconds of response. In testing trends, equal intervals between the logs of Duration were assumed although the distance between the 2- and 6second stimuli is greater than that between other durations. There was also significant habituation across trial blocks. The only *These measures have been described in detail previously (Clifton and Graham, 1968; Graham et al., 1968). Peak Magnitude was the fastest HR per second within a wave of acceleration beginning not later than 3 seconds following stimulus onset and ending when, after two successive decreases, HR either fell below prestimulus level or reversed trend. Peak Latency was the number of seconds from stimulus onset to Peak Magnitude and Response Duration was the number of seconds from the beginning to the end of the acceleration wave. All three indices were computer scored.

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HATTON

TABLE 3 SIGNIFICANT SOURCES OF VARIANCE IN HR SUCCESSIVE ~-SECOND PERIODS FOLLOWING Source

I

df

Durations F D linear F D quad. F Error MS Trial blocks F Error MS Seconds F DXSF Error MS S linear F Error MS TXSF DXTXSF Error MS TS linear F DTS linear F (2 vs. rest) X TS linear F Error MS

II

1.48 0.51 2.75 155.21 10.62** 59.63 77.47** 1.89* 13.61 83.88** 42.01 10.24** 1.84* 8.43 13. oo** 2.05 4.32*

4,95

1,95 1,95 1,95 4,380 16,380 1,95 4,380 16,380 1,95 4,95 1,95

RESPONSE FOR FOUR STIMULUS ONSET III

IV

1.67 0.60 5.68* 343.14 16.55** 169.72 9.98**

1.36 0.33 4.92* 308.79 7.11** 191.45 15 .OS**

1.85 4.82* 1.50 309 27 3.86 166.64 3.19*

8.31 12.49** 26.18 0.97 0.66 5.98 1.24 0.44 -

7.71 20.74** 22.27 1.24 0.35 6.84 1.46 0.24 -

7.52 3.89 23.18 1.45 1.19 6.72 0.62 1.12 -

18.33

20.76

19.17

26.47

*p < .05. **p < .Ol.

SIGNIFICANT

SOURCES

Source Durations F D quad. F Error MS Trial blocks F Error MS T linear F Error MS DXTF (2 vs. rest) X (T, vs. rest) F Error MS *p < .05. **p < .Ol.

OF VARIANCE

df 4,95 1,95 4,380 1,95 16,380 1,380

TABLE 4 IN THREE

INDICES

OF HR

RESPONSE

Peak magnitude

Peak latency

Response duration

1.08 3.28 119.28 2.38 20.65 7.15** 21.58 0.76 3.41

3.21* 7.46** 10.16 2.22 5.46 5.87 6.50 0.63 3.95*

2.43 8.48** 19.65 4.86** 8.75 11.02** 10.33 0.74 4.21*

20.65

5.46

8.75

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275

RESPONSE

6.5 5.5

2 8

350

zP 5

4.5 2.50i

k E

I.50 c

:7---

--.. -.

\ ..-----i

_ __ -.____

Rriod Period Period Period

FIQ. 3. Average HR response during of stimuli varying in duration.

: ‘1 , \ I \

I 2 3 4

successive 5-second periods following

onset

significant component of trend was the linear decrement but the process was not a smooth monophasic decline. Rather, the greatest change was between the first and second trial blocks after which there was gradual waning characterized by alternating periods of increased response. Sokolov (1963) and others have commented on this wave-like process. Changes across seconds were highly significant, especially in the first

l&

f I 2 STIMULUS

I 6 DURATION

I

I

I8 IO (LOG SCALED)

I 30

FIG. 4. Peak Amplitude (in bpm), Peak Latency (in sets.), and Response Duration (in seconds) as a function of differences in stimulus duration.

276

CLIFTON,

GRAHAM,

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5 seconds, confirming the fact that HR variations were not random fluctuations but a response to stimulation, as indicated also by Table 2 showing the significant differences from prestimulus HR. A second question of major concern was whether the course of habituation varied as a function of stimulus duration. The evidence for this was slight. Except during the first response period, none of the pooled interactions of Duration and Trial Blocks were significant, nor were any of the interactions with the orthogonal components of trend. Inspection of response curves suggested that if any differential effects were present they could be ascribed to an absence of habituation to the 2-second stimulus and a relatively uniform habituation to the four longer stimuli. Using the linear component as a measure of habituation, response to the 2-second stimulus did differ significantly from the remaining stimuli during the first period, while the remaining stimuli did not differ from one another. Similar analyses of other periods and of the three indices did not show any further significant differences. Since habituation was not well described by the linear trend, a further analysis was made using the difference between the first, and the remaining trial blocks as a measure of habituation. Peak Latency and Response Duration following the 2-second stimulus again showed significantly less habituation than following the longer stimuli (Table 4). DISCUSSION

Previous studies of the relation between HR response and stimulus duration have yielded apparently discrepant results. While Church et al. (1966) obtained an inverted U-function with shock durations from 0.1 to 10.0 seconds, a monotonic trend was found for similar durations when an air-stream or auditory stimuli were used (Black, 1964; Keen et al., 1965; Steinschneider et al., 1965). These findings might be reconciled on the assumption that nonshock stimuli were less intense than shock and that the less intense the stimulus, the longer the stimulus duration required to give maximal excitatory effects. If the discrepant findings could be explained on this basis, an inverted U-function should appear with nonshock stimulation covering a wider range of durations than that employed previously. The expectation was confirmed by the results of the present experiment. Although not tested, it would also be expected that if the intensity of the auditory stimulation were increased, the inflection point of maximal response would shift to less than 10 seconds. Efforts to determine whether or not the relation of response to stimulus duration changed as a function of repeated stimulation did not yield clear cut results. There was some evidence of greater decrement in

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response to all durations longer than 2 seconds but there was no difference among the four longer durations. These results are in apparent agreement with Koepke and Pribram (1966) who found that the GSR response to a 20-second stimulus was initially longer than that to a 2-second stimulus and that both reached an habituation criterion in the same number of trials. Although these authors concluded that there was no difference in habituation, defined as number of trials to criterion, there must have been greater habituation of response to the 20-second stimulus if habituation is defined as the amount or rate of change in a given period. Bridger (1961) has also reported more rapid habituation with longer stimuli. As Koepke and Pribram (1966) have pointed out, the question of differential habituation as a function of stimulus prolongation is of particular interest because of the hypothesis that prolonging a stimulus produces unconditioned inhibition which can become conditioned to stimulus onset and thus produce habituation (Sokolov, 1960). Greater stimulus prolongation should produce greater inhibition and thus faster habituation; also, decrement in response should first occur near the end of a stimulus and move forward. While results of the present study are compatible with this hypothesis, they do not offer strong support for it. However, Sokolov referred specifically to habituation of the orienting response and it is doubtful that HR acceleration can be so classified. Graham and Clifton (1966) have suggested that HR acceleration is a “defense” or “startle” response rather than an orienting response. A brief comment should be made about the nature of the subjects used in this investigation. Since Church et al. (1966) employed dogs, Black (1964) used rats, and Koepke and Pribram (1966) used adult human Xs, it is assumed that the general findings are not species or age specific. Exact values of parameters would, of course, be expected to vary. In particular, newborns apparently respond with HR acceleration to auditory stimulus intensities that elicit deceleration in adu1t.s (Graham et al., 1968). Accordingly, durations that yield maximal HR acceleration should also vary. REFERENCES APGMZ, V. Current

A

proposal for a new method of evaluation of the newborn infant. Research in Anesthesia & Analgesia, 1953, 32, 260-267. BARTOSHUR, A. K. Response decrement with repeated elicitation of human neonatal cardiac acceleration to sound. Journal of Comparative and Physiological Psychology, 1962, 55, 9-13. BENJAMIN, L. Statistical treatment of the law of initial values (LIV) in autonomic research: a review and recommendation. Psychosomatic Medicine, 1963, 25, 556566.

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BLACK, R. W. Heart rate response to auditory stimuli of varying duration. Psychonomic Science, 1964, 1, 171-172. BRIDGER, W. H. Sensory habituation and discrimination in the human neonate. American Journal of Psychiatry, 1961, 117, 991-996. BRIDGER, W. H., AND REISER, M. Psychophysiologic studies of the neonate: An approach toward the methodological and theoretical problems involved. Psychosomatic Medicine, 1959, 21, 265276. CHASE, H. Habituation of an acceleratory cardiac response in neonates. Unpublished master’s thesis. Univ. of Wisconsin, 1965. CHURCH, R. M., LOLORDO, V., OVERMIER, J. B., SOLOMON, R. L., .~ND TURNER, L. H. Cardiac responses to shock in curarized dogs: Effects of shock intensity and duration, warning signal, and prior experience with shock. Journal of Comparative and Physiological Psychology, 1966, 62, l-7. CLIFTON, R. K., AND GRAHAM, F. K. Stability of individual differences in heart rate activity during the newborn period. Psychophysiology. 1968, 5, in press. D.~vIs, C. M., CROWELI,, D. H., AND CHUN, B. J. Monophasic heart rate acceleration in human infants to peripheral stimulation. American Psychologist, 1965, 20, 478. (Abstract). GRAHAM, F. K., CLIFTON, R. K., AND HATTON, H. M. Habituation of heart rate response to repeated auditory stimulation during the first five days of life. Child Deejelopment, 1968, 39, in press. KEEN, R. E., CHASE, H. H., AND GRAHAM, F. K. Twenty-four hour retention by neonates of an habituated heart rate response. Psychonomic Science, 1965, 2, 265-266. KOEPKE, J. E., AND PRIBRAM, K. H. Habituation of GSR as a function of stimulus duration and spontaneous activity. Journal of Comparative and Physiological Psychology, 1966, 61, 442-448. L.PCEY, J. I. The evaluation of autonomic responses: Toward a grncral solution. Annals of the New York Academy of Science, 1956, 67, 12S-164. LIPTON, El. L., STEINSCHNEIDER, A., AND RICHMOND, J. B. Autonomic function in the neonate. IV. Individual differences in cardiac reactivity. Psychosomatic Medicine, 1961, 93, 472484. M.~LMo, R. B. Activation: a neuropsychological dimension. Psychological Review, 1959, 66, 367386. SOKOLOV, E. N. Neuronal models and the orienting reflex. In M. A. B. Brazier (Ed.), The central nervous system and behavior. New York: Josiah Macy Jr. Foundation, 1960, Pp. 187-276. SOKOLOV, E. N. Perception and the conditioned reflex. New York: Macmillan, 1963. STEINSCHNEIDER, A., LIPTON, E. L., AND RICHMOND, J. B. Stimulus duration and cardiac responsivity in the neonate. Paper presented at biennial meeting of the Society for Research in Child Development, Minneapolis, 1965. WEGNER. N., I\ND ZEAMAN, D. Strength of cardiac conditioned responses with varying unconditioned stimulus durations. Psychological Review, 1958, 65, 238-241.