Startseite Cardiovascular responses to and modulation of pressure pain sensitivity in normotensive, pain-free women
Artikel Öffentlich zugänglich

Cardiovascular responses to and modulation of pressure pain sensitivity in normotensive, pain-free women

  • Christine Mohn EMAIL logo , Olav Vassend und Stein Knardahl
Veröffentlicht/Copyright: 1. Juli 2012
Artikel downloaden (PDF)
Veröffentlichen auch Sie bei De Gruyter Brill
Informationen für Autor*innen Erkunden Sie dieses Fachgebiet
Scandinavian Journal of Pain
Aus der Zeitschrift Scandinavian Journal of Pain Band 3 Heft 3

Abstract

Background and purpose

The psychophysiological responses to and modulation of pressure pain stimulation are relatively new areas of investigation. The aims of the present study were to characterize subjective and cardiovascular (CV) responses to pressure pain stimulation, and to examine the relationship between CV responding and pain pressure pain sensitivity.

Methods

Thirty-nine pain-free, normotensive women were included in the study and tested during the follicular phase of their menstrual cycles. Pain threshold and tolerance were recorded at the right masseter muscle and the sternum, and visual analogue scales (VAS) were used to rate both pain intensity (the sensory dimension) and discomfort (the affective dimension). Mean arterial pressure (MAP), heart rate (HR), and facial and digital skin blood flux (SBF) were registered continuously.

Results

The pain threshold and tolerance were significantly higher at the sternum compared with the masseter, but the level of affective distress was higher at the masseter tolerance point. No associations emerged between pressure pain threshold and tolerance stimulation levels, and the corresponding VAS ratings. Pressure pain stimulation of the masseter induced significant increases in MAP, HR, and a decrease in digital SBF. During sternum pressure stimulation a significant change in HR and digital SBF was observed. There were no significant correlations between CV responding and pressure pain sensitivity.

Conclusion

Healthy women seem to display higher pressure pain sensitivity at the masseter region relative to the sternum. Pressure pain stimulation was associated with significant changes in MAP, HR, and SBF, but was not modulated by CV responses. The validity of these findings is strengthened by our control for menstrual cycle events, weekend-related changes in physiology, and CV changes during pain stimulation.

Implications

This study extends previous reports of SBF sensitivity to electrocutaneous pain into the field of pressure stimulation. Moreover, this study suggests that the often demonstrated association between high BP and low pain sensitivity may not apply to pressure pain specifically. Alternatively, this finding adds to the literature of gender differences in the relationship between CV responding and acute pain sensitivity in general.

Keywords: Blood pressure; Cardiovascular responding; Heart rate; Pain sensitivity; Pressure pain; Skin blood flux

1 Introduction

The mulitidimensional nature of pain perception requires the assessment of several aspects of the pain experience. In order to obtain as complete a picture as possible of the individual’s pain experience, subjective and physiological responses to pain stimulation should be described in addition to the pain sensitivity thresholds. Compared with other stimulation methods such as thermal pain [1], the Subjective and physiological responses to pressure pain are not well known.

As substantiated in previous research, measurements of skin blood flux (SBF) may provide valuable indicators of autonomic nervous system (ANS) activity during psychological challenges [2,3]. Moreover, electrocutaneous pain stimulation seems to trigger increases in facial SBF as well as decreases in digital SBF [4,5]. Similar orofacial SBF changes during pain stimulation have been documented by Kemppainen et al. [6,7]. However, as the research on SBF during pain in humans is relatively new, few studies of SBF responses to experimental pain exist.

In both normotensive and hypertensive individuals, elevations of arterial pressure may be associated with reduced sensitivity to painful stimuli [8,9]. Although the CV–pain relationship appears attenuated or absent altogether in chronic pain groups [10,11], we have recently found that elevated mean arterial pressure (MAP) was associated with reduced pain sensitivity in women with TMD, but not in the pain-free control group [12]. That study employed electrocutaneous and pressure stimulation, whereas the others [10,11] assessed thermal and ischemic pain. Different pain stimulation methods are likely to induce different behavioural, autonomic, and antinociceptive responses [4,13,14].

Moreover, in our previous study of electrocutaneous pain [12] we did not control for certain factors that may modulate pain sensitivity, CV responding or the relationship between those two. These include hormonal effects of menstrual cycle events on pain sensitivity [15] and weekend-related changes in physiology [16]. In addition, the fact that pain stimulation may generate BP increases in its own right could confound the relationship between baseline CVR and subsequent pain sensitivity assessments [17]. Therefore, we control for these factors in the present study.

The general rationale behind this study was to extend previous work on psychological and physiological responding during experimental pain in general to pressure pain stimulation in particular. The primary aim is to characterize subjective and physiological responses, including facial and digital SBF, to pressure pain stimulation. The secondary aim is to examine the relationship between CV responses and pressure pain sensitivity while controlling for possible confounders.

2 Materials and methods

2.1 Subjects

Thirty-nine Caucasian women (see Table 1 for demographic characteristics) were recruited among graduate students of medicine and psychology of the University of Oslo via the students’ mailing lists. Inclusion criteria were age between 20 and 50 years, and ability to speak and understand spoken and written Norwegian. Exclusion criteria (self reported) were known hypertension, chronic pain, general chronic somatic or mental health problems, pregnancy, and use of regular medication apart from oral contraceptives. The subjects were instructed to refrain from drinking alcohol the last 12 h before the experiment, and to avoid drinking tea or coffee, having large meals, and exercising the last 3 h before the experiment. All subjects were tested in the follicular phase of their menstrual cycle in order to rule out pain sensitivity effects of different endogenous reproductive hormone levels [15]. In order to avoid physiological effects of excessive alcohol and/or tobacco consumption during weekends, no experimental testing took place on Mondays [16]. The present study was conducted in accordance with the Helsinki Declaration and approved by the regional Medical Ethics Committee. All subjects gave their informed consent to the participation, and were informed that they were able to withdraw from the experiment at any time. All subjects received a gift-voucher at the price of 250 NOK (approximately USD 45, September 2011) as compensation for time loss.

Table 1

Demographic characteristics.

Age 24.8 (SD 3.9) years
Body mass index 20.9 (SD 3.4)
Regular physical exercise 85.0%
Smoking 15.0%
Married/cohabiting 43.9%
Divorced/separated None
Children living at home 2.4%

  1. Age and body mass index in mean. N=39

2.2 Instruments

Threshold and tolerance of pressure pain: Pressure pain was measured by a pressure algometer (Somedic, Sollentuna, Sweden), with a 1 cm2 diameter probe. The rate of pressure increase is standardized by visual feedback provided by the algometer and was set at 50 kPa/s. Pressure algometry was applied perpendicularly to the central part of the right masseter muscle and the sternum. The subjects were asked to raise their right index finger when the pressure became painful (threshold). Furthermore, the subjects terminated the test by pressing a button when the stimulation became so intense that they wanted to interrupt it (tolerance).

Psychological responses to the pain stimulation: Immediately after each pain stimulation trial, the subjects rated pain intensity (VAS-S, VAS sensory) and discomfort (VAS-A, VAS affective) at threshold and tolerance [13]. This assessment was done by a continuous 100 mm electronic visual analogue scale (eVAS) with the anchors “no pain at all” at the left end and “the worst pain I can imagine” at the right end. The participants rated their pain experience in this way immediately after the pain stimulation trial. They were asked to rate the pain intensity at the threshold level, then pushed the button back to 0, and then rated the pain discomfort at the threshold level, and pushed the button back to 0. The rating of intensity and discomfort at the tolerance level was done in the same manner.

Cardiovascular recordings: MAP and heart rate HR were continuously monitored by the Penñaz method (Ohmeda 2300, Englewood, CO, USA). A cuff containing a photoelectronic sensor was attached to the middle phalanx of the third finger on the subjects’ left hand. The subjects’ hand was placed on a padded armrest in order to keep it positioned at the same level as the heart.

Laser-doppler skin blood flux (LDF) changes were recorded with a Perimed Multichannel Laser Doppler System (PeriFlux 4001 Master, Perimed, Sweden). Miniature probes (Perimed, Sweden) were attached to the left m. masseter area and to the ventral side of the left thumb. This instrument expresses SBF in arbitrary units, proportional to the velocity and concentration of red blood cells moving in the superficial layer of the skin. Although it is customary to present SBF data as percentages of change from baseline, we report the arbitrary levels of flux to be able to perform withinsubject statistical analyses [4].

All signals were AD-converted, recorded, stored and reduced in a computer (Lab View, National Instruments, Austin, TX, USA).

2.3 Procedure

The psychophysiological experiment took place in a sound attenuated and electromagnetically shielded laboratory with the temperature kept constant at 22 °C. The subjects were seated in an upright position in a comfortable, upholstered chair. The experimenter described the function of the instruments and sensors, and was present in the room during the entire experiment. The subjects learned to interrupt the pain stimulation through one trial of pressure pain stimulation at both anatomical sites.

The experiment lasted 30–40 min and consisted of randomized sequences of pressure stimulation at the masseter and sternum. All subjects went through three pressure stimulation trials at the right masseter muscle and three pressure stimulation trials at the right masseter muscle and three pressure stimulation trials at the sternum. Two-minute resting periods between each trial were provided to ascertain that the physiological responses returned to baseline before the next trial.

2.4 Data analysis

All statistical analyses were made using SpSS, release 16 (SpSS Inc., Chicago, IL, USA). The correlations between the three measurements of pain threshold and tolerance at both sites were high (i.e., coefficients in the .68–.89 range, p < .001), with no obvious differences between coefficients obtained from masseter and sternum data. The same pattern emerged from the correlations between corresponding measurements of VAS-S and VAS-A responses. The correlations between the CV response levels during the pain stimulation trials were even higher (i.e., coefficients in the .77–.98 range, p < .001).

Hence, in order to increase the reliability of the measurements, aggregated pain and cardiovascular variables were calculated [18]. An aggregated mean of the three pressure pain stimulations at masseter and sternum served as measures of pain sensitivity. Likewise, aggregated means of MAP, HR, and SBF during the second minute of the three relaxation periods (each lasting 2min) prior to pressure stimulations and MAP, HR, and SBF during the three stimulation trials were calculated. The MAP, HR, and SBF levels during pressure pain stimulation were averaged for the entire stimulation period, which did not last more than 10 s for any subject. Change variables of MAP (Δ MAP) and HR (Δ HR) were computed by subtracting the physiological levels during pre-pain relaxation from the levels reached during the pain stimulation.

The distribution of data was studied by box plots, and tests of skewness and kurtosis. With the sample used in this study, results may be unduly influenced by extreme scorers. In some of the analyses, one or two outliers (i.e., scores 3 SD above or below the mean) were excluded. The number of subjects included in the analyses is indicated in each table.

Differences in pressure and sternum pain sensitivity and VAS responses to the pain were tested with paired-samples t-tests.

Changes in MAP, HR, and SBF from baseline relaxation to pain stimulation were tested with repeated measures ANOVAs with post hoc comparisons.

Pearson’s correlation analyses were run of the relationship between pressure pain thresholds and associated VAS ratings, and between CV responses and pain sensitivity indices. Scatter plots were inspected to obtain a visual image of the correlations. Moreover, in order to provide statistical control for the possible influence of MAP and HR during pain stimulation on the relationship between CV responding and subsequent pain sensitivity [17], partial correlation analyses were conducted with pain-level MAP and HR partialled out.

3 Results

3.1 Pressure pain sensitivity

The masseter pain threshold and tolerance were significantly lower, but the VAS-A ratings higher, than the corresponding sternum stimulation levels (Table 2). No significant relationship emerged between pain threshold and tolerance stimulation levels on the one hand, and the associated VAS ratings on the other (correlations in the r .06–.13 range, all ns).

Table 2

Pressure pain sensitivity.

Masseter Mean (SD) Sternum Mean (SD) t
Pain threshold 214.8(71.7) 375.8(123.1) –10.48[***]
VAS-sensory 3.1 (1.3) 1.6 (0.7) –0.35 (ns)
VAS-affective 3.2 (1.5) 1.3 (0.7) 4.01[***]
Pain tolerance 367.9(130.9) 683.8 (263.9) – 11.07[***]
VAS-sensory 6.2 (1.6) 3.0 (0.9) 0.95 (ns)
VAS-affective 6.3 (1.8) 2.8 (1.0) 2.87[**]

  1. Baseline pain stimulation: the aggregated assessments. Measurement units: kPa (pressure pain), cm (VAS). t = significance test of the difference between masseter and sternum pain sensitivity. ns = non-significant (2-tailed). N = 37–39

3.2 CV responding

As evident from Table 3, statistically significant increases in MAP and HR and significant reductions in digital SBF were observed during pressure pain stimulation compared with baseline.

Table 3

Cardiovascular responding during pressure pain stimulation.

MAP HR SBF face SBF finger
Mean (SD) Mean (SD) Mean (SD) Mean (SD)
Relaxation 107.6 (13.0) 66.7 (9.4) 46.8 (41.2) 204.5 (210.1)
Masseter pain 110.9 (14.5)[#] 72.7 (9.5)[#] 51.1 (45.0) 116.5 (105.8)[#]
Sternum pain 108.8 (13.1) 72.1 (9.3)[#] 47.5 (42.0) 197.8 (199.5)[#]
F 9.99[***] 58.92[***] 2.19 ns 18.22[***]

  1. Pain stimulation: the aggregated assessments. MAP: mean arterial pressure, in mmHg. HR: hear rate, in beats/min. SBF: laser Doppler skin blood flux, in arbitrary units. F: significance test of the differences between relaxation and pain stimulation. ns = non-significant. N=38–39

A series of correlations were run between baseline CV responding and masseter pain sensitivity (Table 4). None of the coefficients that emerged from these analyses were statistically significant.

Table 4

Correlations between CV responding and masseter pain sensitivity.

MAP resting HR resting
Pain threshold .08 .04
Sensory VAS .06 .28
Affective VAS .04 .20
Pain tolerance .11 –.10
Sensory VAS –.02 .25
Affective VAS –.05 .15
MAP during pain stim. HR during pain stim.
Pain threshold .04 .01
Sensory VAS .16 .28
Affective VAS .10 .21
Pain tolerance .03 –.08
Sensory VAS .03 .20
Affective VAS –.02 .12
ΔMAP-pain ΔHR-pain
Pain threshold –.08 –.06
Sensory VAS .26 .02
Affective VAS .16 .02
Pain tolerance –.17 .05
Sensory VAS .12 –.11
Affective VAS .07 –.05

  1. Pearson’s correlation analyse soft he relationship between MAP and HR, pain thresh-old and tolerance, and psychological experience of pain stimulation. Resting: the aggregated relaxation period. ΔMΔP-pain/ HR-pain: change in CVR from the resting period to pain stimulation level. N = 39

Similar correlations were run between baseline CV responding and sternum pain sensitivity (Table 5). Again, none of the coefficients were statistically significant.

Table 5

Correlations between CV responding and sternum pain sensitivity.

MAP resting HR resting
Pain threshold .13 –.14
Sensory VAS –.17 .23
Affective VAS –.14 .29
Pain tolerance .12 –.29
Sensory VAS –.27 .14
Affective VAS –.23 .26
MAP during pain stim HR during pain stim.
Pain threshold .11 –.10
Sensory VAS –.12 .22
Affective VAS –.10 .26
Pain tolerance .10 –.24
Sensory VAS –.27 .09
Affective VAS –.22 .24
ΔMAP-pain ΔHR-pain
Pain threshold .05 .21
Sensory VAS .20 –.07
Affective VAS .17 –.08
Pain tolerance –.01 .22
Sensory VAS –.07 –.07
Affective VAS –.07 .04

  1. Pearson’s correlation analyses of the relationship between MAP and HR, pain threshold and tolerance, and psychological experience of pain stimulation. Resting: the aggregated relaxation period. ΔMAP-pain/ΔHR-pain: change in CVR from the resting period to pain stimulation level. N = 39

The increases in MAP and HR during pain stimulation may influence the relationship between relaxation level CVR and subsequent pain sensitivity. Therefore, MAP and HR levels during pain stimulation were controlled for in partial correlation analyses of the relationship between resting level MAP and HR and pain. However, this procedure did not alter the above results in any statistically significant manner (data not shown).

4 Discussion

The sternum pain threshold and level of tolerance were significantly higher than that of the masseter. Pressure pain stimulation of the masseter induced significant increases in MAP, HR, a decrease in digital SBF, and immediate affective distress. During sternum pressure stimulation a significant change in HR and digital SBF was observed. No support for the modulating role of CV responding on pressure pain sensitivity was found.

4.1 Pressure pain sensitivity

In this study, the sternum pain threshold and level of tolerance were significantly higher than that of the masseter. At the same time, the participants reported significantly more immediate affective distress to the masseter stimulation compared with the sternum pressure. This may explained by the fact that, compared with bone structures, muscular areas may be more sensitive to pain due to being differently innervated by nociceptive structures [19].

There were no significant associations between the pressure magnitude at threshold and tolerance level, and the corresponding VAS ratings of the pain. Moreover, the VAS ratings of affective distress at sternum pressure tolerance level was not even in the moderate range. Possibly, the method of assessing subjective responses to pain not during, but after, the pain stimulation may have biased the assessments.

Alternatively, this is explainable in terms of the VAS method of assessing immediate subjective report of pain intensity and unpleasantness. Other methods, such as the use of numerical rating scales, seem to be more accurate as well as easier to understand [20]. In addition, the VAS method may loose sensitivity at high levels of pain stimulation [21].

4.2 CV responding

We have extended the results of electrocutaneous pain induced digital SBF changes [4] to pressure pain. The finding of non-significant changes in facial SBF coupled with significant digital vasoconstriction during pressure pain is at variance with our previous findings of facial vasodilatation and digital vasoconstriction in parallel during electrocutaneous pain [4]. These divergent results may, however, be due to the different qualities of pain these two types of stimulation induce. The physiological response pattern may vary as to whether the noxious stimulation is inflicted on a superficial (cutaneous) or deep (muscular) region [22]. However, in the absence of systematic studies of physiological response patterns to different types of pain, this suggestion remains somewhat speculative.

4.3 CV modulation of pain sensitivity

Replicating a previous finding [12], the results from this study suggest no significant relationship between CV responding and pressure pain sensitivity in pain-free women. Several methodological aspects strengthen the validity of this finding. We controlled for menstrual cycle events, weekend-related changes in physiology, and the CV changes during pain stimulation.

It may be suggested that pressure pain sensitivity is not as strongly related to CV responding as other types of pain stimulation, e.g., heat pain [10] or ischemic pain [11] have been found to be. Pressure stimulation triggers different nociceptors than do other types of stimulation. Mechanical stimuli such as pressure stimulation, can activate both cutaneous pressure afferents and deeper receptor systems, whereas heat pain, e.g., mainly activate receptors of the skin [22]. Moreover, pressure pain stimulation seems to exhibit a slower return to baseline [22]. The association between CV responding and the different psychophysical and sensory properties of various methods of pain stimulation is still unknown, although the stimulus-dependent nature of the relationship between CV responding and pain sensitivity has recently been suggested by others [23], who found no significant relationship between resting blood pressure and exercise induced muscle pain.

Furthermore, pain from superficial and deep structures seem to trigger separate, integrated patterns of motor, autonomic, and antinociceptive responses [24], coordinated in different parts of the PAG. The dorsolateral PAG triggers a response pattern seen in active responding, i.e., increased arterial pressure, heart rate, and non-opioid analgesia. The ventrolateral PAG controls a response pattern consisting of behavioural inhibition, bradycardia, and opioid hyperalgesia [24]. Superficial pain may evoke irritation and attempts to terminate the stimulation. Pain from deep structures may be associated with rest and immobilization, as would benefit the organism during e.g., inflammation. The topic of defensive responses to different types of pain in humans awaits further elucidation.

Sex differences may be a third explanatory factor. Our participants were women, and women may respond to acute pain and danger primarily through the endogenous opioid system, while men may respond primarily with increases in arterial pressure [10]. In a study of exercise-induced CV increases in pain-free, normotensive men [25], increases in systolic blood pressure was linked to decreases in finger pressure pain sensitivity. However, Bruehl et al. [26] reported that increases in systolic blood pressure was related to decreased ratings of finger pressure pain intensity in a sample consisting of both males and female also when sex was held constant in the analyses.

Alternatively, the ethnic background of the participants in the different studies may be of importance. The present investigation as well as a previous study [12] employed Caucasian females only, whereas other relevant studies [10,11,26] were conducted with a sample of individuals of Afro-American and Asian as well as Caucasian background. Both pain perception and CV responding may show considerable variation across ethnic groups [27,28]. Moreover, the relationship between CV responding and pain sensitivity has been compared across different ethnic groups, with African-Americans not displaying the significant associations between high systolic BP and low pain sensitivity reported in Caucasians [29,30].

4.4 Limitations

When interpreting the results of the present study, certain limitations should be kept in mind. First, all the participants were women. Our findings may not generalize to the male population. Studies elucidating the subjective and physiological responses to pressure pain sensitivity in both men and women are clearly needed.

Second, the sample size was relatively small. It is possible that some of the associations between CV parameters and pain sensitivity would have turned out statistically significant had the number of participants been higher. Therefore, the present results are tentative pending further investigations with a larger sample.

Third, the present study was correlational. Thus, it was not possible to determine the direction of causality between CV responding and pain sensitivity. So far, it has not been possible to decide whether changes in pain sensitivity are causes or consequences of or non-causally related to CV responding.

Fourth, we employed the Penñaz method of measuring MAP and HR. Compared with brachial sphygmomanometry, the finger pressure method may underestimates absolute arterial pressure, but provides accurate measurements of pressure changes [31], which was one of the aims of the present study. Previous relevant studies [10,11,26] did not measure CV parameters continuously. Moreover, brachial sphygmomanometry may generate moderate pressure pain in the subjects, possibly causing interference with the assessment the experimental pain sensitivity that was the aim of our study. Nevertheless, it must be acknowledged that the MAP is influenced more by the diastolic than the systolic pressure, and the systolic pressure seems to be better able to predict pain sensitivity. That our measurements of MAP were not calibrated with pressure values obtained through sphygmomanometry is a limitation of the present study.

5 Conclusion and implications

Healthy women seem to display higher pressure pain sensitivity at the masseter region relative to the sternum. Pressure pain stimulation was associated with significant changes in MAP, HR, and SBF, but do not seem to be modulated by CV responses. The validity of these findings is strengthened by our control for menstrual cycle events, weekend-related changes in physiology, and CV changes during pain stimulation.

This study extends previous reports of SBF sensitivity to electro-cutaneous pain into the field of pressure stimulation. Moreover, this study suggests that the often demonstrated association between high BP and low pain sensitivity may not apply to pressure pain specifically. Alternatively, this finding adds to the literature of gender differences in the relationship between CV responding and acute pain sensitivity in general.

DOI of refers to article: 10.1016/j.sjpain.2012.02.005.

Department of Psychology, University of Oslo, PO Box 1094, Blindern, 0317 Oslo, Norway. Tel.: +47 22 84 51 15; fax: +47 22 84 50 01.

Acknowledgements

Mr Øystein Klingenberg, Mr Shahrooz Elka and Dr Dagfinn Matre were responsible for computer programming and maintenance of the electronic equipment. Ms Kjersti Shani Andersen provided technical assistance in the data-collection phase of the experiment.

References

[1] Loggia ML, Juneau M, Bushnell MC. Autonomic responses to heat pain: heart rate, skin conductance, and their relation to verbal ratings and stimulus intensity. Pain 2011;152:592–8.Suche in Google Scholar

[2] Drummond PD. Facial fiushing during provocation in women. Psychophysiology 1999;36:325–32.Suche in Google Scholar

[3] Drummond PD, Quah SH. The effect of expressing anger on cardiovascular reactivity and facial blood flow in Chinese and Caucasians. Psychophysiology 2001;38:190–6.Suche in Google Scholar

[4] Vassend O, Knardahl S. Effects of repeated electrocutaneous pain stimulation on facial blood flow. Biol Psychol 2005;68:163–78.Suche in Google Scholar

[5] Vassend O, Knardahl S. Personality, affective response, and facial blood flow during brief cognitive tasks. Int J Psychophysiol 2005;55:265–78.Suche in Google Scholar

[6] Kemppainen P, Leppänen H, Jyväsjärvi E, Pertovaara A. Blood flow increases in the orofacial area of humans induced by painful stimulation. Brain Res Bull 1994;33:655–62.Suche in Google Scholar

[7] Kemppainen P, Forster C, Handwerker HO. The importance of stimulus site and intensity in differences of pain-induced vascular refiexes in human orofacial regions. Pain 2001;91:331–8.Suche in Google Scholar

[8] Bruehl S, McCubbin JA, Harden RN. Theoretical review: altered pain regulatory systems in chronic pain. Neurosci Biobehav Rev 1999;23:877–90.Suche in Google Scholar

[9] France CR. Decreased pain perception and risk for hypertension: considering a common physiological mechanism. Psychophysiology 1999;36:683–92.Suche in Google Scholar

[10] Bragdon EE, Light KC, Costello NL, Sigurdsson A, Bunting S, Bhalang K, Maixner W. Group differences in pain modulation: pain-free women compared with pain-free men and to women with TMD. Pain 2002;96:227–37.Suche in Google Scholar

[11] Maixner W, Fillingim R, Kincaid S, Sigurdsson A, Harris MB. Relationship between pain sensitivity and resting arterial blood pressure in patients with painful temporomandibular disorders. Psychosom Med 1997;59:503–11.Suche in Google Scholar

[12] Mohn C, Vassend O, Knardahl S. Experimental pain sensitivity in women with temporomandibular disorders and pain-free controls: the relationship to orofacial muscular contraction and cardiovascular responses. Clin J Pain 2008;24:343–52.Suche in Google Scholar

[13] Price DD. Psychological mechanisms of pain and analgesia. Seattle: IASP Press; 1999.Suche in Google Scholar

[14] Vassend O, Knardahl S. Cardiovascular responsiveness to brief cognitive challenges and pain sensitivity in women. Eur J Pain 2004;8:315–24.Suche in Google Scholar

[15] Riley JL, Robinson ME, Wise EA, Price DD. A meta-analytic review of pain perception across the menstrual cycle. Pain 1999;81:225–35.Suche in Google Scholar

[16] Urdal P, Anderssen SA, Holme I, Hjermann I, Mundal HH, Haaland A, Torjesen P. Monday and non-Monday concentrations of lifestyle-related blood components in the Oslo Diet and Exercise Study. J Intern Med 1998;244: 507–13.Suche in Google Scholar

[17] Caceres C, Burns JW. Cardiovascular reactivity to psychological stress may enhance subsequent pain sensitivity. Pain 1997;69:237–44.Suche in Google Scholar

[18] Rosier EM, Iadarola MJ, Coghill RC. Reproducibility of pain measurement and pain perception. Pain 2002;98:205–16.Suche in Google Scholar

[19] Zylka MJ, Rice FL, Anderson DJ. Topographically distinct epidermal nociceptive circuits revealed by axonal tracers targeted to Mrgprd. Neuron 2005;45: 17–25.Suche in Google Scholar

[20] Gagliese L, Weizblit N, Ellis W, Chan VWS. The measurement of postoperative pain: a comparison of intensity scales in younger and older surgical patients. Pain 2005;117:412–20.Suche in Google Scholar

[21] Duncan GH, Bushnell MC, Lavigne GL. Comparison of verbal and visual analogue scales for measuring the intensity and unpleasantness of experimental pain. Pain 1989;37:295–303.Suche in Google Scholar

[22] Gracely RH. Studies of pain in human subjects. In: McMahon S, Koltzenburg M, editors. Wall & Melzack’s textbook of pain. Edinburgh: Churchill Livingstone; 2005. p. 267–89.Suche in Google Scholar

[23] Poudevigne MS, O’Connor PJ, Pasley JD. Lack of both sex differences and influence of resting blood pressure on muscle pain intensity. Clin J Pain 2002;18:386–93.Suche in Google Scholar

[24] Bandler R, Shipley MT. Columnar organization in the midbrain periaqueductal gray: modules for emotional expression? Trends Neurosci 1994;17: 379–89.Suche in Google Scholar

[25] Koltyn KF, Garvin AW, Gardiner RL, Nelson TF. Perception of pain following aerobic exercise. Med Sci Sports Exerc 1996;28:1418–21.Suche in Google Scholar

[26] Bruehl S, Chung OY, Ward P, Johnson B, McCubbin JA. The relationship between resting blood pressure and acute pain sensitivity in healthy normotensives and chonic back pain sufferers: the effects of opioid blockade. Pain 2002;100:191–201.Suche in Google Scholar

[27] Edwards CL, Fillingim RB, Keefe F. Race, ethnicity and pain. Pain 2001;94:133–7.Suche in Google Scholar

[28] Dimsdale JE. Stalked by the past: the influence of ethnicity on health. Psycho-som Med 2000;62:161–70.Suche in Google Scholar

[29] Mechlin B, Heymen S, Edwards CL, Girdler SS. Ethnic differences in cardiovascular-somatosensory interactions and in the central processing of noxious stimuli. Psychophysiology 2011;48:762–73.Suche in Google Scholar

[30] Mechlin MB, Maixner W, Light KC, Fisher JM, Girdler SS. African Americans show alterations in endogenous pain regulatory mechanisms and reduced pain tolerance to experimental pain procedures. Psychosom Med 2005;67: 948–56.Suche in Google Scholar

[31] Pickering TG, Hall JE, Appel LJ, Falkner BE, Graves J, Hill MN, Jones DW, Kurtz T, Sheps SG, Roccella EJ. Recommendations for blood pressure measurement in humans and experimental animals. Circulation 2005;111:697–716Suche in Google Scholar
Received: 2011-09-09
Revised: 2011-11-25
Accepted: 2011-12-19
Published Online: 2012-07-01
Published in Print: 2012-07-01

© 2011 Scandinavian Association for the Study of Pain

Artikel in diesem Heft

  1. Editorial comment
  2. Spontaneous pain is reduced by conditioning pain modulation in peripheral neuropathy but not in fibromyalgia—Implications for different pain mechanisms
  3. Clinical pain research
  4. Differential pain modulation in patients with peripheral neuropathic pain and fibromyalgia
  5. Editorial comment
  6. Pulsed radiofrequency—Time for a clinical pause and more science
  7. Clinical pain research
  8. Pulsed radiofrequency in peripheral posttraumatic neuropathic pain: A double blind sham controlled randomized clinical trial
  9. Editorial comment
  10. Phantom pains and sensations – how does it feel? Only the patient really knows
  11. Clinical pain research
  12. Phantom phenomena – Their perceived qualities and consequences from the patient’s perspective
  13. Editorial comment
  14. Impact of mental stressor on conditioned pain modulation
  15. Original experimental
  16. The effect of a mental stressor on conditioned pain modulation in healthy subjects
  17. Editorial comment
  18. Pharmacological modulation of chronic pain after whiplash injury
  19. Clinical pain research
  20. Whiplash Associated Disorders (WAD): Responses to pharmacological challenges and psychometric tests
  21. Editorial comment
  22. Why are autonomic responses to pressure pain different from those to heat pain and ischaemic pain?
  23. Original experimental
  24. Cardiovascular responses to and modulation of pressure pain sensitivity in normotensive, pain-free women
  25. Correspondence
  26. Piriformis muscle injection guided by sciatic nerve stimulation: Quick, simple, and safe technique
  27. Correspondence
  28. Musculus piriformis syndrome: Localization and injection therapy—Comment to letter from Mayo-Moldes M et al. [1]
  29. Abstracts
  30. The “pain matrix” reloaded
  31. Abstracts
  32. Endpoints in animal pain models
  33. Abstracts
  34. Evaluating pain-related behavior in spinal cord injury
  35. Abstracts
  36. The role of the amygdala in sensory and emotional-like pain behavior in neuropathic animals
  37. Abstracts
  38. Peripheral and central pain mechanisms—From animal models to clinical research
  39. Abstracts
  40. Human experimental models of central sensitization—Do they bridge the gap between animal models and clinical observations?
  41. Abstracts
  42. Assessment of central sensitization in the clinic. Is it possible?
  43. Abstracts
  44. Migraine neurobiology and treatment
  45. Abstracts
  46. Chronic headaches–Goals and obstacles
  47. Abstracts
  48. Trigeminal neuralgia and other cranial neuralgias
  49. Abstracts
  50. Temporomandibular disorders: Pathophysiology and diagnosis
  51. Abstracts
  52. HIV-associated painful polyneuropathy
  53. Abstracts
  54. Keynote: Neuronal and glial signalling in pain neuroplasticity
  55. Abstracts
  56. Neuropathic pain—From guidelines to clinical practice
  57. Abstracts
  58. Postoperative pain treatment. What’s the evidence—And how to use it?
  59. Abstracts
  60. NSAIDs in postoperative pain
  61. Abstracts
  62. How should we prevent persistent postoperative pain?
  63. Abstracts
  64. Opioids: Genetics and receptors
  65. Abstracts
  66. Chronic pain and sleep disorders
  67. Abstracts
  68. Population-based studies on chronic pain: The role of opioids
  69. Abstracts
  70. Living beyond pain: Acceptance and commitment therapy
  71. Abstracts
  72. Modality specific alterations of esophageal sensitivity caused by longstanding diabetes mellitus
  73. Abstracts
  74. Validation of a porcine behavioural model of UVB induced inflammatory pain
  75. Abstracts
  76. Recovery after a lumbar disc herniation is dependent on a gender and OPRM1 Asn40Asp genotype interaction
  77. Abstracts
  78. Pain sensitivity changes in chronic pain patients with and without spinal cord stimulation assessed by nociceptive withdrawal reflex thresholds and electrical pain thresholds
  79. Abstracts
  80. Acceptance and commitment therapy for fibromyalgia: A randomized controlled trial
  81. Abstracts
  82. Sortilins in neuropathic pain
  83. Abstracts
  84. Systematic review of neuropathic component in persistent post-surgical pain
  85. Abstracts
  86. Pain prevalence in a university hospital in Iceland
  87. Abstracts
  88. The effect of tail-docking neonate piglets on ATF-3 and NR2B immunoreactivity in coccygeal dorsal root ganglia and spinal cord dorsal horn neurons: Preliminary data
  89. Abstracts
  90. Na+/K+-ATPase dependent regulation of astrocyte Ca2+ signalling: A novel mechanism for modulation of long-term pain?
  91. Abstracts
  92. Glutamate attenuates nitric oxide release from isolated trigeminal ganglion satellite glial cells
  93. Abstracts
  94. Acute behavioural responses to tail docking in piglets – Effects of increasing docking length?
  95. Abstracts
  96. Dose and administration-period play a key role in the effect of ceftriaxone on neuropathic pain in CCI-operated rats
  97. Abstracts
  98. Translational aspects of rectal evoked potentials: A comparative study in rats and humans
  99. Abstracts
  100. Time-course of analgesic effects of botulinum neurotoxin type A (BoNTA) on human experimental model of pain induced by injection of glutamate into temporalis muscle
  101. Abstracts
  102. The effect of nerve compression and capsaicin on contact heat evoked potentials (CHEPs) related to Aδ and C fibers
  103. Abstracts
  104. Effect of specific trapezius exercises vs. coordination training on corticomotor control of neck muscles
  105. Abstracts
  106. SNP in TNFα T308G is predictive for persistent postoperative pain following inguinal hernia surgery
  107. Abstracts
  108. Chronic pain in thoracotomy
  109. Abstracts
  110. The variability in thermal threshold-assessments in post-thoracotomy pain syndrome
  111. Abstracts
  112. Persistent pain, sensory disturbances and functional impairment after adjuvant chemotherapy for breast cancer
  113. Abstracts
  114. Neuroplastic alterations in brain responses to painful visceral stimulations reflects individual neuropathic symptoms in diabetes mellitus patients
  115. Abstracts
  116. Exercise and conditioned pain modulation have different effects on cuff pressure pain tolerance in humans
  117. Abstracts
  118. Hyperalgesia in human skin and deep-tissues inside and outside of a UVB irradiated area
  119. Abstracts
  120. Effect of experimental jaw muscle pain on bite force during mastication
  121. Abstracts
  122. Reflex threshold assessment methodology for evaluation of central sensitisation is vulnerable to EMG crosstalk
  123. Abstracts
  124. Cognitive modulation of experimental pain at spinal and cortical levels
  125. Abstracts
  126. Influence of emotionally loaded visual and gustatory stimuli on pain perception
  127. Abstracts
  128. Modulating pain with augmented reality
  129. Abstracts
  130. Offset analgesia: A reproducibility study
  131. Abstracts
  132. Visualization of painful process in peripheral tissue using positron emission tomography and [11C]-D-deprenyl
  133. Abstracts
  134. Mirror-image sensory dysfunction in the post-thoracotomy pain syndrome
  135. Abstracts
  136. Genetic variation in opioid receptor genes and sensitivity to experimental pain in male and female healthy volunteers
  137. Abstracts
  138. Mechanical sensitivity in migraine patients during attack, remission, and pain-free periods:A preliminary study
  139. Abstracts
  140. Multivariate pattern analysis of evoked brain potentials by temporal matching pursuit and support vector machine
  141. Abstracts
  142. Pain following stroke: A prospective study
  143. Abstracts
  144. Chronic thoracic pain in children after cardiac surgery
  145. Abstracts
  146. Chronic pain after breast augmentation is associated with both signs of peripheral nerve injury and central nervous mechanisms
  147. Abstracts
  148. Sensory phenotypes in patients with peripheral neuropathic pain evaluated with quantitative sensory testing
  149. Abstracts
  150. Is health related quality of life related to the pattern of chronic pain?
  151. Abstracts
  152. Comparison between ropivacaine local infiltration analgesia with ketorolac or placebo for total knee replacement surgery
  153. Abstracts
  154. Treatment with topical capsaicin: Experience from a pain clinic
  155. Abstracts
  156. Distribution of concussion related symptoms after whiplash injury in risk strata
  157. Abstracts
  158. HIV/AIDS in different cultures
  159. Abstracts
  160. Pain perception is altered in patients with medication-overuse headache but can improve after detoxification
  161. Abstracts
  162. Detoxification in a structured programme is effective for medication-overuse headache
https://doi.org/10.1016/j.sjpain.2011.12.001
Schlagwörter für diesen Artikel
Blood pressure; Cardiovascular responding; Heart rate; Pain sensitivity; Pressure pain; Skin blood flux

Artikel in diesem Heft

  1. Editorial comment
  2. Spontaneous pain is reduced by conditioning pain modulation in peripheral neuropathy but not in fibromyalgia—Implications for different pain mechanisms
  3. Clinical pain research
  4. Differential pain modulation in patients with peripheral neuropathic pain and fibromyalgia
  5. Editorial comment
  6. Pulsed radiofrequency—Time for a clinical pause and more science
  7. Clinical pain research
  8. Pulsed radiofrequency in peripheral posttraumatic neuropathic pain: A double blind sham controlled randomized clinical trial
  9. Editorial comment
  10. Phantom pains and sensations – how does it feel? Only the patient really knows
  11. Clinical pain research
  12. Phantom phenomena – Their perceived qualities and consequences from the patient’s perspective
  13. Editorial comment
  14. Impact of mental stressor on conditioned pain modulation
  15. Original experimental
  16. The effect of a mental stressor on conditioned pain modulation in healthy subjects
  17. Editorial comment
  18. Pharmacological modulation of chronic pain after whiplash injury
  19. Clinical pain research
  20. Whiplash Associated Disorders (WAD): Responses to pharmacological challenges and psychometric tests
  21. Editorial comment
  22. Why are autonomic responses to pressure pain different from those to heat pain and ischaemic pain?
  23. Original experimental
  24. Cardiovascular responses to and modulation of pressure pain sensitivity in normotensive, pain-free women
  25. Correspondence
  26. Piriformis muscle injection guided by sciatic nerve stimulation: Quick, simple, and safe technique
  27. Correspondence
  28. Musculus piriformis syndrome: Localization and injection therapy—Comment to letter from Mayo-Moldes M et al. [1]
  29. Abstracts
  30. The “pain matrix” reloaded
  31. Abstracts
  32. Endpoints in animal pain models
  33. Abstracts
  34. Evaluating pain-related behavior in spinal cord injury
  35. Abstracts
  36. The role of the amygdala in sensory and emotional-like pain behavior in neuropathic animals
  37. Abstracts
  38. Peripheral and central pain mechanisms—From animal models to clinical research
  39. Abstracts
  40. Human experimental models of central sensitization—Do they bridge the gap between animal models and clinical observations?
  41. Abstracts
  42. Assessment of central sensitization in the clinic. Is it possible?
  43. Abstracts
  44. Migraine neurobiology and treatment
  45. Abstracts
  46. Chronic headaches–Goals and obstacles
  47. Abstracts
  48. Trigeminal neuralgia and other cranial neuralgias
  49. Abstracts
  50. Temporomandibular disorders: Pathophysiology and diagnosis
  51. Abstracts
  52. HIV-associated painful polyneuropathy
  53. Abstracts
  54. Keynote: Neuronal and glial signalling in pain neuroplasticity
  55. Abstracts
  56. Neuropathic pain—From guidelines to clinical practice
  57. Abstracts
  58. Postoperative pain treatment. What’s the evidence—And how to use it?
  59. Abstracts
  60. NSAIDs in postoperative pain
  61. Abstracts
  62. How should we prevent persistent postoperative pain?
  63. Abstracts
  64. Opioids: Genetics and receptors
  65. Abstracts
  66. Chronic pain and sleep disorders
  67. Abstracts
  68. Population-based studies on chronic pain: The role of opioids
  69. Abstracts
  70. Living beyond pain: Acceptance and commitment therapy
  71. Abstracts
  72. Modality specific alterations of esophageal sensitivity caused by longstanding diabetes mellitus
  73. Abstracts
  74. Validation of a porcine behavioural model of UVB induced inflammatory pain
  75. Abstracts
  76. Recovery after a lumbar disc herniation is dependent on a gender and OPRM1 Asn40Asp genotype interaction
  77. Abstracts
  78. Pain sensitivity changes in chronic pain patients with and without spinal cord stimulation assessed by nociceptive withdrawal reflex thresholds and electrical pain thresholds
  79. Abstracts
  80. Acceptance and commitment therapy for fibromyalgia: A randomized controlled trial
  81. Abstracts
  82. Sortilins in neuropathic pain
  83. Abstracts
  84. Systematic review of neuropathic component in persistent post-surgical pain
  85. Abstracts
  86. Pain prevalence in a university hospital in Iceland
  87. Abstracts
  88. The effect of tail-docking neonate piglets on ATF-3 and NR2B immunoreactivity in coccygeal dorsal root ganglia and spinal cord dorsal horn neurons: Preliminary data
  89. Abstracts
  90. Na+/K+-ATPase dependent regulation of astrocyte Ca2+ signalling: A novel mechanism for modulation of long-term pain?
  91. Abstracts
  92. Glutamate attenuates nitric oxide release from isolated trigeminal ganglion satellite glial cells
  93. Abstracts
  94. Acute behavioural responses to tail docking in piglets – Effects of increasing docking length?
  95. Abstracts
  96. Dose and administration-period play a key role in the effect of ceftriaxone on neuropathic pain in CCI-operated rats
  97. Abstracts
  98. Translational aspects of rectal evoked potentials: A comparative study in rats and humans
  99. Abstracts
  100. Time-course of analgesic effects of botulinum neurotoxin type A (BoNTA) on human experimental model of pain induced by injection of glutamate into temporalis muscle
  101. Abstracts
  102. The effect of nerve compression and capsaicin on contact heat evoked potentials (CHEPs) related to Aδ and C fibers
  103. Abstracts
  104. Effect of specific trapezius exercises vs. coordination training on corticomotor control of neck muscles
  105. Abstracts
  106. SNP in TNFα T308G is predictive for persistent postoperative pain following inguinal hernia surgery
  107. Abstracts
  108. Chronic pain in thoracotomy
  109. Abstracts
  110. The variability in thermal threshold-assessments in post-thoracotomy pain syndrome
  111. Abstracts
  112. Persistent pain, sensory disturbances and functional impairment after adjuvant chemotherapy for breast cancer
  113. Abstracts
  114. Neuroplastic alterations in brain responses to painful visceral stimulations reflects individual neuropathic symptoms in diabetes mellitus patients
  115. Abstracts
  116. Exercise and conditioned pain modulation have different effects on cuff pressure pain tolerance in humans
  117. Abstracts
  118. Hyperalgesia in human skin and deep-tissues inside and outside of a UVB irradiated area
  119. Abstracts
  120. Effect of experimental jaw muscle pain on bite force during mastication
  121. Abstracts
  122. Reflex threshold assessment methodology for evaluation of central sensitisation is vulnerable to EMG crosstalk
  123. Abstracts
  124. Cognitive modulation of experimental pain at spinal and cortical levels
  125. Abstracts
  126. Influence of emotionally loaded visual and gustatory stimuli on pain perception
  127. Abstracts
  128. Modulating pain with augmented reality
  129. Abstracts
  130. Offset analgesia: A reproducibility study
  131. Abstracts
  132. Visualization of painful process in peripheral tissue using positron emission tomography and [11C]-D-deprenyl
  133. Abstracts
  134. Mirror-image sensory dysfunction in the post-thoracotomy pain syndrome
  135. Abstracts
  136. Genetic variation in opioid receptor genes and sensitivity to experimental pain in male and female healthy volunteers
  137. Abstracts
  138. Mechanical sensitivity in migraine patients during attack, remission, and pain-free periods:A preliminary study
  139. Abstracts
  140. Multivariate pattern analysis of evoked brain potentials by temporal matching pursuit and support vector machine
  141. Abstracts
  142. Pain following stroke: A prospective study
  143. Abstracts
  144. Chronic thoracic pain in children after cardiac surgery
  145. Abstracts
  146. Chronic pain after breast augmentation is associated with both signs of peripheral nerve injury and central nervous mechanisms
  147. Abstracts
  148. Sensory phenotypes in patients with peripheral neuropathic pain evaluated with quantitative sensory testing
  149. Abstracts
  150. Is health related quality of life related to the pattern of chronic pain?
  151. Abstracts
  152. Comparison between ropivacaine local infiltration analgesia with ketorolac or placebo for total knee replacement surgery
  153. Abstracts
  154. Treatment with topical capsaicin: Experience from a pain clinic
  155. Abstracts
  156. Distribution of concussion related symptoms after whiplash injury in risk strata
  157. Abstracts
  158. HIV/AIDS in different cultures
  159. Abstracts
  160. Pain perception is altered in patients with medication-overuse headache but can improve after detoxification
  161. Abstracts
  162. Detoxification in a structured programme is effective for medication-overuse headache
Jetzt anmelden und 20% sparen
Institutioneller Zugang
Wie funktioniert Authentifizierung?
Haben Sie eine Idee, wie wir unsere Website verbessern können?
Bitte schreiben Sie uns.
© 2025 De Gruyter Brill
Heruntergeladen am 20.10.2025 von https://www.degruyterbrill.com/document/doi/10.1016/j.sjpain.2011.12.001/html
Button zum nach oben scrollen