The relationship between P3-latency and reaction time in depression

THE RELATIONSHIP BETWEEN TIME IN DEPRESSION

Accepted for publication

4 Augut

P3 -LATENCY

19X1

A random series of frcqucnt and infrcqucnt

clicks w;\b presented to 13 primary dcprcs\iws and

I3 hcalthv controls matched for age and gender. Subyxts ax poasiblc in raponsc

AND REACTION

to the infrequent

wcrc instructed

to prcs

3 hutton ;LS fabt

clicks. P3 amplitudes and latencica as uell a\ corrclatlona

betueen P3 latency and reaction time were calculated on a single trial basks using \h’ootl>‘\ adaptilc filter. While reaction tima

wcrc significantly

longer in patients. neither P, latcncio nor P, amplitudc~

diffcrcd between the groups. Thus.

delayed reaction time of depreaivcs sxm~

of impaired

or execution of the motor

selection,

activation,

rcsponw

to he a conacquencc

rnthcr

than of delu\cd

.\timulus evaluation. The correlation between I’, latencv and reaction time U;I\ signlficantl\

\mallcr

in patients than in controls.

1. Introduction One of the core symptoms of the depressive syndrome is motor retardation, often accompanied by delayed reaction times. Possibly, this reflects severity of illness rather than depression for the delay is also found in other psychotic or brain damaged patients (Miller, 1975). We are interested in the question of where the delay in reaction time may take place: in afference or efference. in central processing ~ which may be divided into stimulus evaluation and identification and activation of the correct response (c.f. Teichner and Krebs, 1974) - or in combinations thereof. We tried to approach this question by using auditory evoked brain potentials. In two controlled studies with depressive patients no delay of latencies of brain stem potentials (Bolz. Giedke and Schied, in preparation) or in N, and Pz components of cortical potentials (Giedke, Bolz and Heimann. 1980) was seen. Provided that the potentials investigated are valid measures of afference, the prolongation of reaction time must then take place during stimulus evaluation. response selection, or motor execution. The present study shows that Pj latency, which is considered to be a measure of stimulus evaluation time (Kutas, McCarthy and Donchin, 1977), is not lengthened either. 0301-0511/81/0000~0000/$02.75

0 1981 North

Holland

32

2. Methods 2. I. Subjects The subjects were 13 primary depressive in-patients, diagnosed according to the criteria of Feighner, Robins, Guze, Woodruff, Winokur and Munoz (1972) and 13 healthy controls matched for age and gender without a history of psychiatric illness (c.f. table 1). Nine of the patients and all controls had been free of psychotropic medication for more than 6 days. 2.2. Experimental

procedure

The subject was seated in a comfortable armchair in an electrically shielded and sound-attenuated chamber. Recording and evaluation were performed in a neighbouring room from which the subject could be observed. Firstly, two tones of identical intensity (70 dB) and duration (100 msec, risetime 8 msec, falltime 2 msec) but different frequencies (1000 and 1150 Hz) were presented binaurally via earphones to the subject. He was then instructed as follows: ‘As soon as you are sure that you hear a high-pitched tone, press the key as fact as possible. You don’t need to pay attention to the low-pitched tones. After this, a Bernoulli series of the two tones was presented with a constant interstimulus interval (ISI) of 5 sec. The low pitched (non target) tone occurred with a probability of p = 0.8; the high-pitched (target) tone with a probability of p = 0.2. 2.3. Recording The EEG was recorded from Cz and Pz (lo-20 system) to linked mastoids (A ,, A,); the EOG from the outer canthi (upper left to lower right). Ag-AgCl electrodes were used. T.C. was 2.5 set, high frequency cut-off 30 Hz (-3 dB). 2.4. Sampling Sampling at a rate of 625 Hz began 400 msec before tone onset and continued for 1640 msec. The computer (Nicolet Med 80) collected 16 target and 60 non-target tones to which the subject had responded correctly and which were free of ocular artifacts (i.e. EOG-activity < 80 PV within the sampling interval). After each accepted EEG period connected with a target tone four periods with non-target tones were sampled. Thus, because of possible habituation, it was ensured that potentials to target and non-target tones had about the same position in the experimental series.

Patients Controls

Table I Experimental

Age

42i9 4219

m

6 6

”

13 13

subjects

2Oi-6

Hamilton depression (I 7 items) score

v. Zerssen depression-score (D-S, self-rating)

2x 16 2=2

v. Zerssen mood xore @f-S. self-rating)

41*12 IO-’ 8

2.5. Identification

of ERP components

Each subject’s EEG and EOG was averaged synchronous to the stimulus (SSA) and separately for targets and non-targets. For better identification of P3 components, the EEG was low pass filtered (5 Hz, ~ 3 dB) using a simple digital filter as described by Ruchkin and Glaser (1978). For statistical computations (cf. table5 in section 3.2) amplitudes of N,. P2, and slow negativity (for definitions see below) were based on unfiltered averages; for N, and P3 amplitudes and all latencies the filtered data were used. 2.5.1. Definitions Baseline: average of the EEG from -400 msec to tone onset. N,: most negative value of the AEP between 50 and 150 msec (after onset). PZ: most positive value between 150 and 240 msec. N,: most negative value after P2 between 200 and 300 msec. P3: most positive value after N, between 250 and 840 msec. Slow negativity: mean EEG-amplitude between 500 and 1238 msec. N, /Pz amplitude: Pz -N,. N, /P3 amplitude: P3-N,.

tone

2.5.2. Woody filter In order to identify latencies of single P3 components to target tones we applied a cross correlational technique suggested by Woody (1967). First, the conventionally averaged EEG as well as each single trial of the raw EEG was digitally low pass filtered (Butterworth-type, 7 Hz, -3 dB) to eliminate (Yactivity which might surpass the component of interest (i.e. q7). Then, a section of the averaged EEG, from 200 to 1020 msec post-stimulum, was used as a template to which an identical section of each filtered raw EEG was cross correlated by moving the template in steps of 1.6 msec across it. All single sweeps reaching cross correlation coefficients larger than 0.5 within time lags of * 220 msec were then shifted on the basis of their respective time lags. All other sweeps were left in their original positions. Averaging of all sweeps shifted and nonshifted resulted in a new template. This process was repeated with each new template until the average gain -in maximum cross correlation (Ar) sank below 0.03, which was the case after two to five iterations. For correlation of individual P3 latencies and reaction times all sweeps were used, i.e. also those which correlated less than 0.5 with the template and/or reached their maximum correlation at time lags exceeding ~220 msec. 2.5.3. Response gwchronized uveruges Finally, response synchronized averages EEGs to target tones.

(RSA)

were

computed

for the

Herein, P3 was defined as the most positive peak in the entire period; slow negativity (SN) as the average amplitude in the 200 msec following onset of reaction, as indicated by a switch closure.

3. Results 3.1. Reuction times The comparatively long reaction times and the small number of errors show that the subjects took care to work accurately rather than fast. As expected, the depressed patients reacted significantly slower than controls. In number of errors, the difference was not statistically significant (c.f. table2). The four patients treated with psychotropic drugs did not differ from the rest of the patients’ group, neither in reaction time nor in number of errors. 3.2. Stimulus

synchronized

merages

(SSA)

Fig. I shows examples of stimulus synchronized EEG averages for a patient and a control. In most averages N,, P2, and P3 were clearly visible: less frequently this was also true for N, and SN. Thanks to artifact rejection, ocular movements were rare and did not influence the EEG record considerably. Tables 3 and 4 show mean and standard deviation of amplitudes and latencies of the five potentials identified (c.f. also fig. 2). A two way ANOVA with repeated measures (corresponding to target and non target tones) (table 5) reveals mainly effects of condition (i.e. target vs. non-target): The amplitude of N,. N,/Pz. N, (Cz only), P3 (Pz only), N2/q?. and SN (Cz only) are larger to targets than to non targets. Latency of N, is shorter to targets. The two experimental groups differ only in N, latency at Cz for which a group X condition interaction is also to be seen: Patients’ N, to non targets appears later than that of controls (t = 2.966, d.f. = 26, 2p < 0.01). Table 2 Choice reaction

times and errors

Reaction time (msec) Number of errors Misses Fakes Total

Patients (n= 13)

Controls (n= 13)

U-Test

510’105 (,z=ll) 1.5 ? 2.li 4.2’-

427 ‘X5 (!I= I I) 0.5-t 0.x 0.6’ 0.Y 1.0-t 1.0

2p
I .6 5.4 6.3

ll.h. “.S. n.s.

cz Nf

p3

l-l

non-forget

(frequent)

(4

PZ

non-target

(b) cz Nl

Urequentl

37

(d) Fig. 1. Stimulus

CI

synchronized

EEG averages

-

Nl

of a patient

WNTROLS PATIENTS

non-target

-

(a.b) and a control

(frequent)

CONTROLS PATfENTS

12’OOmsec

non-target

Fig. 2. Stimulus

synchronized

group

axrages

(frequent)

comparing

patients

and controls

(c, d))

3X

The results concerning N, latency are to be interpreted with caution. Nz is not easy to identify, for it often overlaps with 91. The effects mentioned are only found at Cz, not at Pz and are no longer present after Woody filtering (see section 3.3). There is a tendency for the patients to differentiate better between rare and frequent tones as measured in Nz/Px amplitude (both leads) and P3 amplitude (Cz only). However, in ANOVA this does not manifest itself in a signficant group X condition interaction (F;,,,,, = 3.1/3.2/3.3/, p < 0.1). 3.3. WOOL& filtering In Woody filtering the EEG responses to target tones increases N, and P? amplitudes by 20-40 percent (see fig. 5). As in the unfiltered values. N, is larger at Cz (patients 7.3 pV, controls 7.4 pV) than at Pz (3.6.3.6) whereas P3 is larger at Pz (15.0, 14.2) than at Cz (10.5, 11.5). There are no significant group differences, neither in amplitude, nor in latency. Corresponding, in both groups the Pj latency corrections (in msec) are also similar (Cz: patients 68.9 + 24.1. controls 55.4 * 19.9; Pz: patients 69.9 t 26.3, controls 70.9 i- 28.4). 3.4. Relutiomhip

hetK,een

P_, Iutency

und reaction

time

For each experimental subject the P? latencies to single target tones were rank correlated with the corresponding reaction times (Spearman’s rho. n = 16).

,

“A

cz

_I

3-

, -

0

2.

_’

-

Pz

I

PATIENTS (n--131

-

-

-

-

1.

-02 -01

“A 3.

1

02 06 de’ ,OI 00 OA 0.3 0.5 0.7 0 9 , 0.1 5

1.

-0.2

I I

n

CONTROLS (n-131

--

a0

Of

53 0.2

lrl

of rank correlation

15, 04

0.6

d7

0.0

d.9; 1'0

-

I

I ; I

--

as 0.6 -OS2 r a0 0.2 a4 -01 1 01 0.3 0.5 0.7 0.9 0.9r, I

Fig. 3.Distributian

.oY,

I

I I

2.

.I

I

-

r-In

-

-Tl

-0.3 -0.1 , 0.1 0.3 0.5 0.7 dsr, -0.2 OD 0.2 04 0.6 0.8 I

coefficients

(,;) for the relation

P,-latency/reaction

time.

Table 4 Mean and standard (c.f. 2.5).

deviation

of ERP latencies

(msec, SSA). All values arc haxd

on filtered data

cz N,

p2

N2

p3

Patients Targets Non-targets

I lY.62 i 7.26

220.69 2 19.73 22X.3X f 15.00

251.77’10.5’) 27O.OOi23.70

347.23 + 25.6% 36X.00-c 109 02

Controls Target.\ Non-targets

123.54’12.57 122.151 7.0’)

231.3X~ll.00 234.46 -t IO. I5

24X.00 + 13.52 247.77 + 12.9X

412.Y2flXI.OX 3XX.OX+ 132. IO

120.00 i

7.45

PATIENTS

Fig. 4. Reaction-synchronized

group averages

for targets

41

pz N,

N2

p2 227.38i21.45

243.X5?

X.26

353.31~

27.54

116.0X-tII.15

231.54-r13.7X

252.77-t 17.X6

366.15"

73.73

llY.69i 11.75

230.X52 17.6X

242.46%

llY.OO~l3.42

236.46-t 7.00

245.85-t 7.53

116.692

9.39

7.X1

39X.92-' 131.X7 37Y.69?

73.42

For each EEG lead and each experimental group, this yielded 13 rank correlation coefficients, the distribution of which is shown in fig. 3. For n = 16, r, is significantly different from zero if it exceeds 0.50. Significant r;-values for Cz (Pz) were found for two (0) patients and four (4) controls. Fig. 3 shows that at Cz and Pz five of the patients had negative and eight positive coefficients, (i.e. the mean does not significantly differ from zero, sign-test). In the control group, however, all coefficients but one are positive (2~ < 0.01, sign-test). Accordingly, the distributions of r;-values for patients and controls prove to be significantly different from each other (2~ < 0.05, U-test). In other words, there is a significantly closer coupling between P3 latency and reaction time in healthy controls than in depressive patients. 3.5. Reuction synchronized

averages (RSA)

In the RSA (fig. 4) only Pj and SN can be seen clearly. Compared to SSA, P3 amplitudes are smaller (though they are not low-pass filtered) but mean amplitudes of SN are larger. This suggests that P3 is related more closely to the stimulus than the motor response and vice versa, SN to the motor reaction rather than to the stimulus. Table6 shows mean and standard deviation of Pj amplitudes and latencies and mean amplitudes of SN in RSA. There are no group differences in either of these variables.

4. Discussion Our experiment consisted of a go-no-go choice reaction task. A motor reaction was required in reponse to the rarely occurring (target) stimuli only.

42

Table 6 Mean

and standard

deviation

of P3 and SN amplitude5

of rcaponac sychronizcd

averages: PA

latency is mcasurcd in relation to mean reaction time P,-amp.

(pV)

(msec)

~ 226.

I -c22x.

SN (wL)

Patient>. Cz

3.97~

Controls,

5.02 pi 6.05

~ 141.5 1244.3

Patients. Pz

7.5 I 4 7.45

~- 101.3 + 158.2

Controls.

Y.35-‘5.lY

Cz Pr

6.93

PJat.

-63.7

I

-t 144.X

-Y.36

7.15

-8.36

4 6.20

1.1% +5.73 0.052 + 5.6X

Frequent (non-target) stimuli demanded no motor reaction. Both kinds of stimuli elicited the well-known event-related potential components N,, Pz, N, and P3; a slow negativity (SN), following P? at Cz does not seem to correspond to the often reported slow wave, as the latter is negative frontally and positive parietally (Squires, Squires and Hillyard, 1975; Roth, Ford and Kopell, 1978). Our SN was present for more than 0.5 set, was negative centrally and near zero parietally; it was larger in the response-synchronized averages than in the stimulus-synchronized averages, thus probably being a phenomenon which accompanies the motor act, possibly the N, wave of Gerbrandt (1978). However, as we were not able to record from more than two electrodes (Cz and Pz) because of technical limitations and were applying one experimental design only we could not evoke and/or sharply discriminate between closely adjoining or overlapping components (e.g. N, sac, P3 aab, different P2s and slow negativities, for review see Picton and Stuss, 1980). This would be a major drawback in the case of q7, the identification of which was at the centre of our interest. As our experiment was designed to elicit a P,b, and the average latencies (340-410 msec) as well as the limited topography (Pz > Cz) were in accordance with reported features of Pjb (Squires et al. 1975) we feel justified to consider it a P,b indeed. The amplitudes of N, (Cz), P3 (Pz) and SN (Cz) were higher in response to target than to non-target stimuli, which is in accordance with the results of many other investigators. That the same holds true for N, amplitudes (Cz and Pz) is at variance with several studies summarized by Hillyard, Picton and Regan (1980, p. 291). Obviously, some sort of stimulus evaluation beyond stimulus set selection (Hillyard et al., 1980) can already show up in N, amplitude. The condition effect on P3 amplitude was small and reached significance only at Pz. In our opinion this is mainly due to the relatively large interstimulus interval (ISI). In support of this hypothesis Thier, Giedke and Bolz (in preparation) show that the difference between P3 amplitudes which developed in response to infrequent/relevant or frequent/irrelevant stimuli depends on

the ISI~smaller ISIS resulting in increasing amplitude differences. Furthermore, the small number of trials allowed subjects little time to learn that targets are infrequent and non targets frequent (c.f. Johnson and Donchin, 1980). Finally, the fact that the target signals were relatively frequent ( p = 0.2) may have added to this effect. There was no condition effect on the latencies of N,, P2, and P3, but there was for N1 (at Cz). As the significant group and group by condition effects in the ANOVA and the significant c-tests testify, this statistical effect can be attributed to the patients’ longer N2 latencies in response to non-target stimuli. As N, is a small wave, wedged between Pz and PX, its amplitude and latency are more prone to artifactual distortion by the algorithm used to identify it (c.f. 2.5) than those of the larger components. Therefore we won’t emphasise this finding. The negative or ‘hold’ responses to non-target tones can be considered mismatch judgments, which, in turn, are supposed to yield longer reaction times than match judgments (Tueting, 1978). If one acknowledges the potential role of N, in triggering reaction time (Bostock and Jarvis, 1970; Ritter, 1978) the delay in N2 latency may make sense. It is not clear, however, why only the patient’s group shows this effect. Our main interest was focussed on the group differences. With the exception of the longer N, latencies in patients just mentioned and a marginal group by condition interaction for NZ/Ps and P3 amplitudes there are no group effects whatsoever, neither in the unfiltered nor in the filtered data. This is somewhat surprising, for there have been several reports of reduced N, and Pz amplitudes of auditory evoked potentials in depressives (for review c.f. Shagass, Ornitz, Sutton and Tueting, 1978; Giedke et al., 1980). So far we know of only two experiments in which a P3 paradigm has been applied to depressive patients. Levit, Sutton and Zubin (1973) report on N, /P3 amplitudes which do not differ between depressives and controls. Goodin, Squires and Starr (1978) and Squires, Goodin and Starr (1979) in a study on demented patients, also report in passing on P3 latency in four and five depressives, respectively, but refer to N, and Pz components only summarily as being the same in all groups. In view of the meagre direct experimental evidence we can only speculate that the more demanding task of a P3 paradigm reduces or levels out the differences seen in other settings, e.g. when subjects were just listening to tones or performing reactions in the course of a simple CNV paradigm as was the case in the studies done and quoted by Shagass et al. (1978) and Giedke et al. (1980). Levit et al. (1973) as well as Squires et al. (1979) did not find differences in amplitude and latency of P3 between depressive patients and controls. This is in accordance with the present data. Also if Woody filtered data are compared, the groups differ neither in amplitude and latency of Pj nor in variability of Pj latency.

Because there is ample evidence of Pi latency and amplitude being associated with stimulus evaluation (for review c.f. Donchin, Ritter and McCallum. 1978; Tueting, 1978) we can conclude that stimulus evaluation is not delayed in our depressive patients. The delay in reaction time (510 msec as compared to 430 msec in controls) must be a result of retarded selection, activation, or execution of the motor response. In other words: depressives seem to have impaired access to the executive motor programs. Correlutiot7

hetn*eetz P, lutetyv

utd

reuction

time (r. t.)

To determine the correlation between Pj latency and reaction time on a single trial basis there are several methods in use. The simplest way is to detect a component by sight, an approach which lacks explicitness. Therefore we preferred to make use of the Woody filter (Woody, 1967) one of various cross-correlational techniques. The main problem with Woody filtering is that there will be, as a rule, more than one component in the time section to which the filter is applied. Therefore, the selection of the appropriate time window is crucial. It should be large enough to include the component of interest, which. in the case of Pj is known to vary substantially in latency, but also small enough to exclude as many other components as possible. Inspection of the individual SSA (fig. 1, for example) utilized as templates for the filtering procedure clearly demonstrated that P3 is the predominant component in the time window selected (see also fig. 5). As the Woody procedure tends to align the largest peaks of the single sweep and the template, the resulting time shift will be mainly determined by this component. Other components which are not time locked to the predominant peak will be attenuated. Elimination of a-activity is a necessary prerequisite for Woody filtering because a-peaks may surpass the component of interest. A digital Butterworth lowpass with a 7 Hz breakpoint seemed adequate because it guarantees substantial a-reduction without considerably affecting the long latency components. For the formation of new templates in the Woody procedure relatively strict criteria were applied. Only such single sweeps were shifted in time which had a maximal cross correlational coefficient with the template of at least 0.5 within a maximum time lag of k220 msec. In this way the danger of deforming the template by other components, was reduced, though not entirely ruled out. A larger time window of 820 msec was applied for the computation of the individual P3 peak latencies as their possible range should not already be restricted beforehand - especially in view of the large variability of reaction times to which they were to be correlated. To correlate ‘false’ Pj latencies to reaction times seems to be a minor risk as any correlation would thereby be reduced rather than increased. The precautions don’t absolutely guarantee that we have actually identified P,-peaks-the less so as one has to think of so far undiscovered neurophysio-

CONTROLS P3 Lb0

logical processes taking p lace in this or another time window. With this qualification, the relationship between Pj latency and reaction time will now be discussed. If the psychological construct of stimulus evaluation is to have any meaning in a choice reaction task, some part of the underlying physiological processes must occur early enough to precede a correct response. In our control group the P3 peak precedes the motor reaction by an average of 30 msec - too short to represent its trigger (Ritter. Simson and Vaughan, 1972). Often, Pi latency is even longer than r.t. (for review see Donchin et al., 1978; Tueting. 1978). This means that stimulus evaluation must start before the Pj peak, e.g. at the beginning of the P? wave (Ritter et al., 1972) or at N, (Bostock and Jarvis.

1970; Ritter,

1978), or even at N, (cf. the present results). It seems reasonable to assume at least two stages in stimulus evaluation: a late one, represented by the P3 peak, and an earlier one, preceding and probably triggering P3 as well as the motor reaction. This could explain the varying correlations which have been found between P3 latency and r.t. If there are any processes with a variable time course common to both Pi and motor reactions, positive correlations between the two events are to be expected. Indeed, all averaged Pj -r.t. correlations reported are positive or near zero, never negative. The longer time a process takes, the more vulnerable it is to disturbance by confounding variables. Therefore, the P,-r.t. correlation must be a function of r.t., P3 latency, and the position as well as the duration of the physiological processes common to both events (i.e. the earlier and shorter the common processes and the longer the r.t. and P3 latency the smaller the P,-r.t. correlation). In our experiment the Pj-r.t. correlations are rather low in the controls but comparable to those of other investigators (Pfefferbaum, Ford. Roth and Kopell, 1980a, b). Our patients, who exhibit significantly longer r.t. also show significantly smaller (near zero) PX-r.t. correlations. Taking both groups together, there is rank correlation of r, = -0.49 (p
al., 1980). and P3 amplitude, which is subject to the perceived probability of the stimulus (Johnson and Donchin, 1980), are not reduced. There is even a tendency for patients to differentiate better between target and non target tones as measured by N2/P3 amplitudes (both leads) and PX amplitude (Cz only) (group by condition interaction p < 0.1). All this and last but not least P3 latency itself as a measure of the speed of stimulus evaluation strongly suggest (even though they do not prove) that depressives are as attentive and motivated as the controls-at least for the task reported here. This conclusion was also reached by Bruder and coworkers from experiments on the effect of auditory shadowing on reaction times (Bruder. Sutton, Babkoff, Gurland, Yozawitz and Fleiss. 1975; Bruder, Yozawitz, Berenhaus and Sutton, 1980). In contrast to depressives. schizophrenics did not benefit from the shadowing-possibly an analogue to their small P3 amplitude (c.f. Levit et al., 1973: Shagass et al., 1978; Roth, Pfefferbaum, Horvath and Kopell. 1980).

Acknowledgement

We are indebted computation.

to Helga Pimp1 for her valuable

assistance

in recording

and

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