Psychophysiological reactivity of migraine sufferers in conditions of stress and relaxation

JournaloJW~choromorrc Pnnted tn Great Rnrain

Receorch. Vol. 32. Nos 415. pp. 48.WY2.

0

PSYCHOPHYSIOLOGICAL SUFFERERS

BIRGIT

IYXX

REACTIVITY

IN CONDITIONS RELAXATION

KR~NER-HERWIG,

DIRK RENATE

(Received 12 Januaryl988;

OF MIGRAINE

OF STRESS

DIERGARTEN,

DAGMAR

M22-3WY/8K $3.00 + .OO IYXX Pergamon Press plc

AND

DIERGARTEN

and

SEEGER-SIEWERT

accepted in revised form 23 June 1988)

Abstract-The assumption of a specific migraine-related psychophysiological response stereotype under conditions of stess, recovery and relaxation was examined in 37 migraineurs (nonheadache state) and 44 normal controls. Two stressors were presented, industrial noise and a ‘social discomfort’ situation, each was followed by a recovery period. Relaxation was induced by verbal instructions accompanied by soft music. The following physiological measures were assessed: pulse volume amplitude (frontotemporal and digital), skin temperature (fronto-temporal and digital) and skin resistance responses. Results showed no group differences in responses to the stressors. Physiological recovery from stress was delayed in migraineurs in the electrodermal parameter. During relaxation, migraineurs showed less digital vasodilation than the controls. Overall, physiological and subjective responses differed between the two stressors. The hvnothesis of a soecific vasomotor stress resoonse stereotvoe in mieraineurs could not be .. corroborated. The observed differences in relaxation and recovyry were Hypothesized. But the overall results are not easily explained on the grounds of a coherent model (e.g. elevated sympathetic arousal level).

INTRODUCTION BEGINNING with the early studies of Wolff et al. [l-3] empirical data have accumulated supporting the view that the pathophysiological basis of migraine is a cranial vascular dysfunction. The painful migraine attack is correlated with excessive vasodilation, probably intra- and extracranial [4]. Whether a vasoconstrictive phase always precedes the vasodilation is still controversial. Nevertheless, no physiological theory has been able to explain satisfactorily what starts the dysfunctional process ending in a migraine attack and what predisposes an individual to this disorder. On the basis of clinical data [5] the hypothesis was developed that migraine is the consequence of a specific vascular stress response stereotype. This response specificity in the non-headache state could give way to a migraine attack under special not yet known circumstances. The response specificity of migraineurs may be limited to the cranial region or be more general, i.e. comprise cranial and peripherul vasculature. Appenzeller et al. [6], as well as other researchers, assume that the autonomic nervous system plays an important role in these processes. Furthermore, Feuerstein and Gainer [7] and Andrasik et al. [S] point out that migraineurs may have a deficit in recovering from stress. Additionally it is proposed that migraineurs tend to have a dysfunctional relaxation response.

Department

of Psychology,

University

of Diisseldorf, 483

F.R.G

Various studies were conducted to examine the hypothesis of a vascular response specificity in migraineurs during S~YE.SS (8-151 and under co~~ditio~~ oj‘non-nversice .stimidution [ 16201. A close analysis of these different studies gives very controversial evidence regarding the gcnerrrl issue of response specificity. Furthermore, contradictory results refer to the pafteun of physiological response stereotype. Relatively few studies are concerned with the processes of recovery after stress and relrrxation 18. 12, 211, so that there is no definitive evidence on this issue. Also, the question of the importance of sympathetic overarousal (as indexed by nonvascular autonomic measures) has not yet been decided [7, 22-241. Avoiding some of the methodological shortcomings of other experiments, we decided to study the problem of a specific psychophysiological reactivity in migraineurs by using the following experimental procedures: (1) Extracranial vasomotor processes and peripheral vasomotor processes were assessed simultcmeoluly. (2) Photoplethysmographic methods for the assessment of vascular processes were used. Skin temperature, often regarded as a measure of vascular activity, was additionuliy assessed. (3) The laboratory stressors used were devised to be of some external validity. (No artificial strcssors such as white noise or backward counting were used.) The stressors represented different types of stress (physical/psychological). (3) Post-stress periods (recovery periods) were included in the design. (5) Relaxation behavior was assessed. (6) A measure of general sympathetic arousal was taken. The following main hypotheses were to be tested; migraineurs differ from headache-free controls: (1) They respond with a more distinct estrucnmial and peripherrrl vusoconstriction to stress, i.e. we expect a more pronounced stress or defensive response in both vascular systems 1251. (2) In the recovery period. migraineurs respond by more pronounced vasodilation in the rxtrcicrunial vessels and show less vasodilation in the peripheral vessels. Furthermore. we expect a higher level of electrodermal activity. We thus assume an extracranial regulatory dysfunction (overshooting response) and a deficit in is also reflected in the next sympathetic arousal reduction. This assumption hypothesis. (3) During relaxation migraineurs show a marked extracranial vasodilation and no or less vasodilation in peripheral vessels. METHOD Ss were rrcr-uitecl by a local nrwspaprr announcement informing them of the research project on migraine and the possibility ot receiving non-pharmacological treatment (biofeedback) after participating in the study.

The group consisted of 77 fem,lle [X = 11 .-I yr (S.D. = IO.h)] and IO malt [x = 33.3 yr (S.D. = I I.?)] migr;tincurs. Thq were told ihal they \verc to pxticip;itc in ciiffercnt diagnostic procedures before therapy, including a psychoph~siologic;ll laboratory session.

Psychophysiological

reactivity

485

in migraineurs

The control group included headache-free Ss [33 female, 2 = 33.7 yr (S.D. = IO.?): I I male. 2 = 39.X yr (S.D. = I I.Y)], who were recruited within the campus. Most of them were paid for participation in the headache research project. It would have been desirable to add a second control group to the design. conG5ting of tension headache sufferers. in order to be able to differentiate these theoretically different headache types from each other unti from normal controls. However, our capacity to supply the headache patients with therapy was limited. so that we had to abandon this additional research problem. There is no statistical difference in sex between the two group\. but wc have a higher a\crapc ape in the migraine group (x’ = 12.8, p < 0.01). All Ss were informed not to take any medication the day before the session and not to drink coffee or smoke on the day of the experiment. Two stressful situations were presented 10 each S. These were a noise stresaor and a social discomfort situation. The physical stressor consisted of industrial noise from ten different sources. e.g. welding apparatus, automatic grinder. circular >aw. etc. The average intensity of these noises differed between 79 and Y3.Y db(A). The total exposure time was 8 min. The second stressor was de\lgned to provoke ‘social discomfort’ by focusing a video camera on the Ss’ faces. who were told that they were observed in an adjacent room. Reasons for this procedure were not given. To render the situation more credible. Ss were able to view their own faces for 2 min on a monitor in the experimental room. Furthermore. the camera zoom was adapted several times during the 8 min of exposure. The order of presentation of streasors was permutated. so that half of the subject\ of each group was first exposid to the noise, half of them to the social dl?comfort situation. The subjective strcssfulne\F of these procedures was tested with students before the study. Each stressor was succeeded by a 4.min recovery period. Because of methodological reason\ relating to the physiological variables. various baseline periods were included (\ee Tahle I).

TAHI e I.-Sequence Periods

Baseline I Relaxation I Baseline 2 Stressor A’ Recovery A Rating Relaxation 2 Baseline 3 Stressor B Recovery B Rating

’ t

Stressors (noise/social First 16 PVA of every $ Value\ taken every 30 3 Number of SCR >().I

Duration (min) 2 8 2 8 4 5 8 2 x 4 .5

of periods in session and data extraction Numher

of data points extracted

PV~,,:,,,

T , lid,

I; (BS) 4 (RX) I 4 (S) 2 (RC)

4;: I6 4 16 8

7% 8 2

3 I6 8

2

I (see above) 4 (see above) 2 (see above)

discomfort) were permutated. second minute were averaged and expressed set and expressed in ‘% of baseline. r*ho.

EDA

4

3

in % of baseline.

Furthermore the session included two relaxation periods. Only the first relaxation period wa\ analysed. since it preceded the \tresaor presentation and could therefore not be influenced by it. The second relaxation period was introduced to ensure that arousal wa\ reduced when presenttng the second stressor. Relaxation was induced by asking the Ss to listen to a tape with verbal relaxation instructions accompanied hy soft guitar music. Again, these periods lasted for 8 min. Two rating periods lvere inserted. where Ss were asked about their discomfort during stressor presentation. The following physiological variables were registered throughout the session: pulse volume amplitude taken from the left fronto-temporal artery (PVA,), pulse volume amplitude taken from the phalange of the left hand thumb (PVA,,). skin temperature taken from the left temporal site of the skull (T,). I pho) taken from the palmar site of the left hand (EDA). A photoplethysmographic method [2h] was applied, in which In f r :I - red light was projected onto the blood vessels of the akin. The hackscattercd light. which is modulated by blood volume change. i\ dctcctcd by a photodiode and converted into a current signal with its peak-to-peak amplitude reflecting the blood volume pulse (BVP). The R-wave of the ECG was taken to trigger the beginning of a time

BIRGIT KRONER-HERWIG et al

486 Table Source

II.-Analysis df 1

Group Stressor Periods GxS GxP SXP GxSxP

1 5 1 5 5 5

of variance PI’.& ns 20.74: ns ns n$ 13.61$ ns

(group

Source

EDA

Group Period

ns 11.54: (df=7) ns

GxP * P 4.10;

F-scores

T.

T,,

3.? * 2.39* ns

ns ns ns ns

ns 19.28$ 3.71t

4.& ns

of variance

x period):

PVA,

* p < 0.10; f p < 0.05; : p < 0.01. Periods: 5 SI~_J, RCl_z (see Table I); selection ” periods: RCImJ.

TABIJX III.-Analysis

x stressor

(group

IIS

ns 3.43 ns

21:;3!: ns of temperature

x period)

pVA<, 2.66* 3.91; (df=4) ns

measures

PVA,

ns h.Ol$ (df=4) ns

ns 6.71: (df=l) ns

(df”)

2.80X (1) 5.97: (I) 2.YYi’ (4) ns (1) 5.37 $- (4) ns (4) ns (4)

simultaneous

in the first relaxation _. Id

EDA

to PVA.

period T,

ns ns (df=4) ns

t p < 0.05: $ p < 0.01,

TABLE IV.-Discomfort

rating

of stressors

No

Some

Rating Average

MIG CO

18 18

8 21

5 4

3 0

3 0

MIG (‘0

1 4

Y 3

3 16

I3 1s

9 5

Strong

Very strong

Stressor Social discomfort Noise

window for extracting signal samples which were averaged over 16 heart cycles to extract mean BVP values [for further details see ref. 271. The thermocoupler was calibrated to 25-37°C and was correct within a limit of 0.1%. Room temperature was held constant (25°C + 0.5%). Electrodermal activity was registered by a 1.2 constant voltage AC-coupler. Ss were asked to evaluate the stressors on a S-point discomfort scale (see Table IV). Including attachment of measuring devices, adaptation period and time for instruction, the session lasted for nearly 2 hr.

RESULTS

Because photoplethysmography renders no absolute data the responses are expressed in terms relative to baseline measures of each period. This was also done with the temperature values, since our recorder guaranteed no absolute measurement (small pen deviations from 0 level to the beginning of registratinnj. The ED.4 variable was defined as number of responses per minute. Various analyses of variance, performed on each stress, recovery and relaxation period and each physiological variable. confirmed that there were no differences

Psychophysiological

reactivity

487

in migraineurs

(except for one single case) between the order ofpresentation of the two different stressors. So the main analysis leaves this factor unconsidered. In order to test the main hypotheses, statistical analyses of variance were performed by a multifactorial partly dependent design on each physiological variable separately. Univariate analysis was chosen, because we were interested in the specific response characteristics of each variable in the two groups. If necessary, F-tests for repeated measures were corrected by the Greenhouse-Geisser method (which is routinely provided by the BMDP programme). Analysing the stress and recovery effects, the follokng factors were considered: ‘group’ (migraine/control), ‘stressor’ (noise/social discomfort) and ‘period’ (see Table 11). Analysis of the EDA was limited to the recovery periods (see Table II) because the reactive ‘orienting’ components of the EDA during stressor presentation were mingled with the ‘spontaneous’ EDA activity.

PVA % 0

PVAd

.

PVAt

-

noise

-- - sot. dis.

Migraine

Stress [Recovery1 FIG.

1 .-Pulse

volume

amplitude

(digital,

temporal) recovery

in migraine periods.

and control

subjects during stress and

BIRGI I KROVFR-HERWIC; ct cd.

488

There were no differences between groups, either in the vascular variables (PVA,IPVA,,) or in the temperature measures (T,I7’,,) during presentation of stressors (Figs 1, 2). In all but one variable, differences between the two stressors could be observed (see Table II). Noise led to a vasoconstrictive response in the PVA,,. whereas there was a tendency towards vasodilation in the social discomfort situation. PVA, tended to behave in the same direction. Digital temperature. too, showed a clearly different behavior in the two situations. It decreased during noise and remained near baseline or even increased during the social discomfort situation. Temporal temperature did not vary much at all (Fig. 2). In all variables a stressor x period interaction effect was found, which points to pronounced variations in the peripheral vasomotor and temperature variables during the presentation of noise (growing constriction and cooling). Disregarding the EDA for a moment. the peripheral vasomotor function is the only physiological variable showing a certain recovery effect, especially after noise (reduced vasoconstriction). though the values do not reach baseline level. In no case could we observe a group-specific process. The EDA (Fig. 3) is the only variable that differentiates between groups (on the 10% significance level) in the recovery periods. This main effect is specified by a group x period interaction (see Table II). Migraine Ss have a higher EDA

o

.

Td Tt

noise - - - sot. dis.

\

b

Psychophysiological

rwctivity

in migraineurs

EDA (f) noise D sot. dis. l

2-

1-

cl Baseline

Olj/ FIG. 3.-Electrodcrmal

activity in migraine

1

Recovery

t

and control subjects during baseline and rccovcry

periods.

response level. They show no recovery from stress but even irlcremse their EDA after stress. On the other hand the control Ss decrease their EDA, as could be expected, due to deactivation of the sympathetic system. This pattern is found after noise and social discomfort. The relaxation data were separately analyzed by a two factorial design (group/ period, see Table III; Fig. 4). Analysis of the relaxation data results in only one group effect (at the 10% significance level). As expected, the migraineurs tended to respond by digital vasoconstriction whereas the controls showed some degree of peripheral vasodilation. The PVA, showed a tendency towards vasodilation in both groups. A correlational analysis of vascular and temperature data by non-parametric Spearman rank analysis was performed. The two different stress situations and the relaxation period were analysed separately. Since the temporal relations between the vascular and temperature processes are not known, various correlational analyses with a time lag between variables up to 27O’sec were performed. Each group of Ss was analyzed separately. The highest positive correlation coefficients were found in the control group during relaxation. Here the PVA,, and the r,, correlation coefficients reached a level of r = 0.52-0.65, which is highly significant. Most other coefficients were of very small range and were non-significant. Interestingly enough, various negative coefficients were observed, especially within the migraine group and especially between the cranial measures of pulse volume amplitude and temperature. Temperature varied with a minimal time lag of +60 set relative to the vascular responses. After each stress period, subjects had rated their ‘discomfort’ induced by the situation. There were no differences between the groups either in the social discomfort or in the noise situation, but there was a difference in the evaluation of

490

BIRGIT KRONFR-HERWIC;

er crl

TEMP

PVA

A

%

-

MIORAINE

----

CONTROL

C’

110

i? ; 100

-

: m

.-_---_._---_-.-_

T1

‘-___ t

P”Ad

90

0

FIG.

4.-Pulse

-10

II-

Relaxation

volume

the two different social discomfort

amplitude

stressors. situation

Relaxation

and

skin temperature in migraine relaxation periods.

The noise was more (see Table IV).

stressful

and control

\uhjects

to the subjects

during

than the

DISCUSSION

There were no significant differences between groups in their physiological Our main hypothesis of a vascular stress response responses to the stressors. specificity in migraineurs therefore could not be corroborated. Migraineurs did not show more vasoconstriction (peripheral and extracranial) during stress as was predicted on the basis of the expected very pronounced defensive response. Nor did they respond by a distinct extracranial vasodilation as part of an overshooting negative feedback process in the extracranial vessels after stress. On a purely descriptive level, though, the migraine sufferers demonstrated a wider range of reactivity in the extracranial artery (especially a marked vasoconstriction during exposure to noise). The predicted differences in vasomotor functioning between migraineurs and control in the recovery periods were not found. Furthermore the hypothesis of higher sympathetic arousal was only partly supported. Regarding electrodermal activity as an index of autonomic arousal, we found evidence for inability of migraineurs to reduce arousal after stress as we predicted. This. however, is not seen in the peripheral vasomotor variable. There was a borderline effect in our data relating to the expected deficit of migraineurs in their ability to relax. Here the peripheral vascular variable

Psychopysiological

reactivity

in migraineurs

4Yl

differentiated the groups but electrodermal activity did not. The predicted excessive vasodilation in the extracranial artery, however. was not seen in the migraineurs during relaxation. Not quite expectedly, we observed a stressor specific response pattern in both groups. Considered physiological and subjective data this finding is interpreted as a failure of the psychological ‘stressor’ (social discomfort) to really induce pronounced stress in most subjects. Thus. the observed response pattern is possibly not due to the different types of stressors but to diffcrcnt intensity of induced stress. This also would signify that we only had one ‘real’ recovery period. The parallel assessment of pulse volume amplitude and skin temperature in both sites (extracranial and digital) gave important information, even considering the low II in each group. Skin temperature is often taken as a direct reflection of vasomotor functioning. Our data. especially the correlational analyses give some evidence that this assumption is not warranted, especially for the extracranial vasomotor functioning. The PVA reflects the activity of the frontal-temporal artery, whereas the temperature most probably reflects blood flow in the smaller skin vessels. Following this line of argument. negative correlations found in the migraine group may point to the fact that there is dissociation of blood flow in the big extracranial arteries and small skin vessels in migraineurs. Though our study gave mainly negative evidence regarding the hypothesis of a specific physiological stress and relaxation related response pattern in migraineurs we would suggest further examination of this issue. Stressors should be of longer duration and greater psychological impact. Furthermore, the process of recovery should be studied for a longer period. Relaxation behavior could be examined more thoroughly using different deactivation strategies.

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SOVAK M, DALESSIO D, KUNZEL M, STERNBACH R. Physiological and psychological changes accompanying biofeedback training. In: Pain (Edited by BONIC.~ J). New York: Raven Press, 1980. SOKOI.OV YN. Perception and the Conditioned Reflex. New York: Pergamon Press, 1963. BROWN CC. Methods in Psychophysiology. Baltimore: Williams and Wilkins, 1967. FALKENSTEIN M, HOORMANN J, WEITKAhwERJ. ZULCII J. Signalverarbeitung bei photoelektrischer GefaRplethysmographie. Riomed Technik 1984; 29: 213.