The genetic underpinnings of right-wing authoritarianism and social dominance orientation explain political attitudes beyond Big Five personality.

OBJECTIVE: Political attitudes are predicted by the key ideological variables of right-wing authoritarianism (RWA) and social dominance orientation (SDO), as well as some of the Big Five personality traits. Past research indicates that personality and ideological traits are correlated for genetic reasons. A question that has yet to be tested concerns whether the genetic variation underlying the ideological traits of RWA and SDO has distinct contributions to political attitudes, or if genetic variation in political attitudes is subsumed under the genetic variation underlying standard Big Five personality traits. METHOD: We use data from a sample of 1987 Norwegian twins to assess the genetic and environmental relationships between the Big Five personality traits, RWA, SDO, and their separate contributions to political policy attitudes. RESULTS: RWA and SDO exhibit very high genetic correlation (r = 0.78) with each other and some genetic overlap with the personality traits of openness and agreeableness. Importantly, they share a larger genetic substrate with political attitudes (e.g., deporting an ethnic minority) than do Big Five personality traits, a relationship that persists even when controlling for the genetic foundations underlying personality traits. CONCLUSION: Our results suggest that the genetic foundations of ideological traits and political attitudes are largely non-overlapping with the genetic foundations of Big Five personality traits.

Stability and Change in Biopsychosocial Factors Associated With Fatigue 6 and 12 Months After Traumatic Brain Injury: An Exploratory Multilevel Study.

OBJECTIVE: To explore factors associated with stability and change in fatigue from 6 to 12 months following traumatic brain injury (TBI). SETTING: Combined in- and outpatient acute care and postacute rehabilitation settings. PARTICIPANTS: A total of 103 patients with confirmed intracranial injury were assessed 6 and/or 12 months following TBI. DESIGN: A prospective observational study with repeated measures at 2 time points, analyzed with a hybrid mixed-effects model. MAIN MEASURES: Primary outcomes were the fatigue factor derived from items from several fatigue patient-reported outcome measures (PROMs; Fatigue Severity Scale, Chalder Fatigue Scale, Giessen Subjective Complaints List-fatigue subscale, and Rivermead Post-Concussion Symptoms Questionnaire-fatigue item) Secondary outcomes were PROMs relating to pain, somatic and psychological distress, insomnia, sleepiness, personality traits, optimism, resilience, behavioral activation and inhibition, and loneliness, as well as neuropsychological measures. Demographic variables and injury severity characteristics were included as covariates. RESULTS: In multilevel regression, female sex, years of education, and 3 factors related to injury severity, somatic vulnerability, and psychosocial robustness were all significantly associated with variation in fatigue between subjects, and explained 61% of the variance in fatigue that was due to stable between-subject differences. Fatigue levels declined significantly over time. Changes in pain severity, somatic symptom burden, psychological distress, and behavioral inhibition were positively associated with changes in fatigue, explaining 22% of the variance in fatigue within subjects. CONCLUSIONS: The study demonstrated that several previously implicated factors show robust effects in distinguishing individuals with TBI on levels of fatigue, but only a few show additional within-subject associations across time. Pain severity, somatic symptom burden, psychological distress, and behavioral inhibition correlated with fatigue across time, implicating these factors as crucial targets for rehabilitation of patients with TBI who suffer from persistent fatigue.

The role of neuroticism and pain in dental anxiety: A twin study.

OBJECTIVES: Accumulating evidence has revealed that dental anxiety is robustly associated with dental care-related pain and discomfort, but also with the personality trait of neuroticism (i.e. the relatively stable disposition to experience the world as distressing, threatening and unsafe). However, there is a near absence of research on these risk factors in samples for which genetic information is available. With the aim of arriving at a more refined understanding of dental anxiety, this twin cohort study assessed genetic and environmental influences on neuroticism, dental care-related pain and dental anxiety, and the relation between these phenotypes. METHODS: Participants were recruited from the Norwegian Twin Registry, and data collections were carried out in 1992-98 (Time 1) and 2011 (Time 2). Well-validated questionnaires were used to assess the study variables, including Corah's Dental Anxiety Scale, the Numerical Pain Rating Scale, the NEO Personality Inventory Revised (Time 2) and Eysenck's Personality Questionnaire (Time 1). Pearson correlation analysis and generalized estimating equations (GEE) were used to investigate phenotypic associations. Analyses of genetic and environmental influences were performed using Cholesky modelling. RESULTS: A total of 746 monozygotic (MZ) and 770 dizygotic (DZ) twins in the age group of 50-65 participated in the study. Moderate estimates of heritability for dental anxiety (0.29), treatment-related pain (0.24) and neuroticism (0.45-0.54) were found. Cholesky modelling showed furthermore that neuroticism assessed at Time 1 and Time 2 was related to dental anxiety and pain via both genetic and individual-specific environmental pathways, albeit not very strongly. The particularly high phenotypic correlation observed between dental care-related pain and anxiety (r = .68) was explained by both overlapping genetic and individual-specific environmental influences (the genetic and environmental correlations were .84 and .63 respectively). CONCLUSIONS: The findings provide deeper insight into the aetiology of dental anxiety and confirm that while it is strongly linked to treatment-related pain experiences, this relation is to a considerable degree independent of general negative affectivity/neuroticism.

Justice sensitivity is undergirded by separate heritable motivations to be morally principled and opportunistic.

Injustice typically involves some people benefitting at the expense of others. An opportunist might then be selectively motivated to amend only the injustice that is harmful to them, while someone more principled would respond consistently regardless of whether they stand to gain or lose. Here, we disentangle such principled and opportunistic motives towards injustice. With a sample of 312 monozygotic- and 298 dizygotic twin pairs (N = 1220), we measured people's propensity to perceive injustice as victims, observers, beneficiaries, and perpetrators of injustice, using the Justice Sensitivity scale. With a biometric approach to factor analysis, that provides increased stringency in inferring latent psychological traits, we find evidence for two substantially heritable factors explaining correlations between Justice Sensitivity facets. We interpret these factors as principled justice sensitivity (h2 = 0.45) leading to increased sensitivity to injustices of all categories, and opportunistic justice sensitivity (h2 = 0.69) associated with increased sensitivity to being a victim and a decreased propensity to see oneself as a perpetrator. These novel latent constructs share genetic substrate with psychological characteristics that sustain broad coordination strategies that capture the dynamic tension between honest cooperation versus dominance and defection, namely altruism, interpersonal trust, agreeableness, Social Dominance Orientation and opposition to immigration and foreign aid.

Impact of Somatic Vulnerability, Psychosocial Robustness and Injury-Related Factors on Fatigue following Traumatic Brain Injury-A Cross-Sectional Study.

Fatigue is a common symptom after traumatic brain injuries (TBI) and a crucial target of rehabilitation. The subjective and multifactorial nature of fatigue necessitates a biopsychosocial approach in understanding the mechanisms involved in its development. The aim of this study is to provide a comprehensive exploration of factors relevant to identification and rehabilitation of fatigue following TBI. Ninety-six patients with TBI and confirmed intracranial injuries were assessed on average 200 days post-injury with regard to injury-related factors, several patient-reported outcome measures (PROMS) of fatigue, neuropsychological measures, and PROMS of implicated biopsychosocial mechanisms. Factor analytic approaches yielded three underlying factors, termed Psychosocial Robustness, Somatic Vulnerability and Injury Severity. All three dimensions were significantly associated with fatigue in multiple regression analyses and explained 44.2% of variance in fatigue. Post hoc analyses examined univariate contributions of the associations between the factors and fatigue to illuminate the relative contributions of each biopsychosocial variable. Implications for clinical practice and future research are discussed.

The role of pain and psychological distress in fatigue: a co-twin and within-person analysis of confounding and causal relations.

OBJECTIVE: Fatigue is a common symptom in somatic and mental illness. Musculoskeletal pain and psychological distress have in turn frequently been shown to be associated with fatigue across clinical conditions and in the general population. The study aims to disentangle direct effects from those due to mere confounding from shared etiologies. DESIGN: The study used genetically informative longitudinal twin data, through a co-twin control design with an additional within-person dimension. METHODS: Data on fatigue, pain and distress from 2196 mono - and dizygotic twins from the Norwegian Twin Registry examined at two time points five years apart was analyzed using multilevel generalized linear regression modeling. Fatigue was regressed on pain and distress, with further controls added for confounding from genetic and stable non-shared environmental sources. RESULTS: Pain and distress had a significant impact on fatigue at genetic, stable non-shared environmental and time-varying levels, even when controlling for somatic comorbidity. CONCLUSION: The findings indicate that a significant proportion of the association between fatigue, pain and distress is due to genetic and environmental confounding. Pain and distress exert significant, albeit smaller effects on fatigue even when controlling for genetic and stable environmental contributions, indicating direct effects. Potential etiological pathways and underlying mechanisms are discussed.

Dentist-administered cognitive behavioural therapy versus four habits/midazolam: An RCT study of dental anxiety treatment in primary dental care.

The study aimed to test the effectiveness of cognitive behavioural therapy (CBT) administered by a general dental practitioner (GDP) in a general dental practice. In a two-arm parallel randomised controlled trial, the experimental group received a short dentist-administered CBT-intervention (D-CBT). A best-practice control group (FHM) received dental treatment during sedation with midazolam combined with an evidence-based communication model (The Four Habits Model). Ninety-six patients with self-reported dental anxiety were allocated to the treatment arms at a 1:1 ratio. Modified Dental Anxiety Scale (MDAS) scores spanned from 12 to 25, and 82 patients (85%) had a score of 19 or more, indicating severe dental anxiety. In both treatment arms, scores on MDAS and Index of Dental Anxiety and Fear (IDAF-4C) decreased significantly, but no differences were found between treatment arms. Mean reductions were: MDAS scores: -6.6 (SD = 0.5); IDAF-4C scores: -1.0 (SD = 1.1). In conclusion, local GDPs in general dental practices with proper competence have the ability for early detection of dental anxiety and, with the use of a manual-based D-CBT or FHM treatment, GDPs could offer efficient first-line treatment suitable for dental anxiety of varying severities.

Correlations between social dominance orientation and political attitudes reflect common genetic underpinnings.

A foundational question in the social sciences concerns the interplay of underlying causes in the formation of people's political beliefs and prejudices. What role, if any, do genes, environmental influences, or personality dispositions play? Social dominance orientation (SDO), an influential index of people's general attitudes toward intergroup hierarchy, correlates robustly with political beliefs. SDO consists of the subdimensions SDO-dominance (SDO-D), which is the desire people have for some groups to be actively oppressed by others, and SDO-egalitarianism (SDO-E), a preference for intergroup inequality. Using a twin design (n = 1,987), we investigate whether the desire for intergroup dominance and inequality makes up a genetically grounded behavioral syndrome. Specifically, we investigate the heritability of SDO, in addition to whether it genetically correlates with support for political policies concerning the distribution of power and resources to different social groups. In addition to moderate heritability estimates for SDO-D and SDO-E (37% and 24%, respectively), we find that the genetic correlation between these subdimensions and political attitudes was overall high (mean genetic correlation 0.51), while the environmental correlation was very low (mean environmental correlation 0.08). This suggests that the relationship between political attitudes and SDO-D and SDO-E is grounded in common genetics, such that the desire for (versus opposition to) intergroup inequality and support for political attitudes that serve to enhance (versus attenuate) societal disparities form convergent strategies for navigating group-based dominance hierarchies.

Genetics, personality and wellbeing. A twin study of traits, facets and life satisfaction.

Human wellbeing is influenced by personality traits, in particular neuroticism and extraversion. Little is known about which facets that drive these associations, and the role of genes and environments. Our aim was to identify personality facets that are important for life satisfaction, and to estimate the contribution of genetic and environmental factors in the association between personality and life satisfaction. Norwegian twins (N = 1,516, age 50-65, response rate 71%) responded to a personality instrument (NEO-PI-R) and the Satisfaction With Life Scale (SWLS). Regression analyses and biometric modeling were used to examine influences from personality traits and facets, and to estimate genetic and environmental contributions. Neuroticism and extraversion explained 24%, and personality facets accounted for 32% of the variance in life satisfaction. Four facets were particularly important; anxiety and depression in the neuroticism domain, and activity and positive emotions within extraversion. Heritability of life satisfaction was 0.31 (0.22-0.40), of which 65% was explained by personality-related genetic influences. The remaining genetic variance was unique to life satisfaction. The association between personality and life satisfaction is driven mainly by four, predominantly emotional, personality facets. Genetic factors play an important role in these associations, but influence life satisfaction also beyond the effects of personality.

Fatigue symptoms in relation to neuroticism, anxiety-depression, and musculoskeletal pain. A longitudinal twin study.

BACKGROUND: The nature of the relationship between fatigue and its risk factors is poorly understood. In the present study the genetic and environmental association between anxiety-depression, musculoskeletal (MS) pain and fatigue was examined, and the role of neuroticism as a shared risk factor that may possibly explain the co-occurrence between these phenotypes was investigated in a combined cross-sectional and longitudinal twin design. METHODS: The sample consisted of 746 monozygotic (MZ) and 770 dizygotic (DZ) twins in the age group of 50-65 (mean = 57.11 years, SD = 4.5). Continuous measures of fatigue symptoms and the other phenotypes were employed. Using Cholesky modeling, genetic and environmental influences on the phenotypes, and the associations among them, were determined. Analyses were performed using measures of neuroticism obtained concurrently and 13-19 years earlier. RESULTS: Results from multiple regression analyses showed that neuroticism, anxiety-depression symptoms, and MS pain were all significantly associated with fatigue, controlling for sex, education, and general health indices. The best-fitting biometric models included additive genetic and individual-specific environmental effects. Heritabilities in the 0.40-0.53 range were demonstrated. Furthermore, while there was a considerable overlap in genetic risk factors between the four phenotypes, a substantial proportion of the genetic risk shared between anxiety-depression and fatigue, and between MS pain and fatigue, was independent of neuroticism. CONCLUSION: Evidence for a common underlying susceptibility to report fatigue symptoms, genetically linked to neuroticism, anxiety-depression, and MS pain, was found. Both unique and pleiotropic effects appear to be involved in the genetic architecture of the phenotypes.

Musculoskeletal complaints, anxiety-depression symptoms, and neuroticism: A study of middle-aged twins.

BACKGROUND: Musculoskeletal (MS) complaints are reported commonly, but the extent to which such complaints reflect the severity of site-specific pathology or a more generalized susceptibility to feel pain/discomfort is uncertain. Both site-specific and more widespread MS conditions have been shown to be linked to anxiety and depression, but the nature of this relationship is poorly understood. In the present study the role of neuroticism as a shared risk factor that may possibly explain the co-occurrence between anxiety-depression and MS complaints was investigated. METHOD: The sample consisted of 746 monozygotic and 770 dizygotic twins in the age group of 50-65 years (M = 57.11, SD = 4.5). Using Cholesky modeling, genetic and environmental influences on neuroticism, anxiety-depression and MS symptoms, and the associations among these phenotypes were determined. RESULTS: A single factor accounted for about 50% of the overall variance in MS symptom reporting. The best-fitting biometric model included sex-specific additive genetic and individual-specific environmental effects. All 3 phenotypes were strongly influenced by genetic factors, heritability (h2) = 0.41-0.56. Furthermore, while there was a considerable overlap in genetic risk factors among the 3 phenotypes, a substantial proportion of the genetic risk shared between MS complaints and anxiety-depression was independent of neuroticism. CONCLUSION: Evidence for a common underlying susceptibility to report MS symptoms, genetically linked to both neuroticism and anxiety-depression symptoms, was found. (PsycINFO Database Record

A clinimetric analysis of the Hopkins Symptom Checklist (SCL-90-R) in general population studies (Denmark, Norway, and Italy).

BACKGROUND: Although the Symptom Checklist (SCL-90-R) is one of the most widely used self-reported scales covering several psychopathological states, the scalability of the SCL-90-R has been found to be very problematic. AIMS: We have performed a clinimetric analysis of the SCL-90-R, taking both its factor structure and scalability (i.e. total scale score a sufficient statistic) into account. METHODS: The applicability of the SCL-90-R has been found acceptable in general population studies from Denmark, Norway and Italy. These studies were examined with principal component analysis (PCA) to identify the factor structure. The scalability of the traditional SCL-90-R subscales (i.e. somatization, hostility, and interpersonal sensitivity) as well as the affective subscales (i.e. depression and anxiety and ADHD), were tested by Mokken's item response theory model. RESULTS: Across the three general population studies the traditional scaled SCL-90-R factor including 83 items was identified by PCA. The Mokken analysis accepted the scalability of both the general factor and the clinical SCL-90-R subscales under examination. CONCLUSION: The traditional, scaled, general 83 item SCL-90-R scale is a valid measure of general psychopathology. The SCL-90-R subscales of somatization, hostility, and interpersonal sensitivity as well as the affective subscales of depression, anxiety, and ADHD were all accepted by the Mokken test for scalability, i.e. their total scores are sufficient statistics.

Five-factor personality traits and pain sensitivity: a twin study.

Factors underlying individual differences in pain responding are incompletely understood, but are likely to include genetic influences on basal pain sensitivity in addition to demographic characteristics such as age, sex, and ethnicity, and psychological factors including personality. This study sought to explore the relationship between personality traits and experimental pain sensitivity, and to determine to what extent the covariances between these phenotypes are mediated by common genetic and environmental factors. A sample composed of 188 twins, aged 23 to 35years, was included in the study. Heat pain intensity (HPI) and cold-pressor pain intensity (CPI) ratings were obtained using standardized pain testing procedures, and personality traits were assessed with the NEO Personality Inventory, Revised. Associations between personality and the pain sensitivity indices were examined using zero-order correlations and generalized estimating equations. Bivariate Cholesky models were used in the biometric analyses. The most robust finding was a significant phenotypic association between CPI and the personality facets Impulsiveness (a facet of Neuroticism) and Excitement-Seeking (a facet of Extraversion), and estimates of the genetic correlation were .37 (P<.05) and .43 (P<.05), respectively. In contrast, associations between HPI and personality seemed weak and unstable, but a significant effect of Angry Hostility (a facet of Neuroticism) emerged in generalized estimating equations analysis. Although the genetic correlation between these phenotypes was essentially zero, a weak but significant individual-specific environmental correlation emerged (re=.21, P<.05). Taken together, these findings suggest that CPI is more consistently related to personality dispositions than HPI, both phenotypically and genetically.

Neuroticism and self-reported somatic health: a twin study.

Using a twin sample (N = 188; 53 monozygotic and 39 dizygotic twin pairs, and 4 single twins whose co-twin did not participate), this study sought (1) to estimate heritabilities of neuroticism and of somatic complaints rated on the basis of two different time frames ('the last week' vs. 'in general'); (2) to estimate the genetic association between neuroticism and the complaints indices and (3) to examine to what extent somatic complaints are aetiologically distinct from neuroticism. Using models with common additive genetic (A) and individual-specific environmental (E) factors, the heritabilities for neuroticism and complaints 'in general' and during 'the last week' were 0.46 (0.20-0.65), 0.44 (0.22-0.62), and 0.45 (0.22-0.63), respectively. Nearly 60% of the phenotypic correlation between neuroticism and somatic complaints were accounted for by A. Furthermore, a substantial part of the variance in somatic complaints was due to unique genetic and individual-specific environmental influences unrelated to neuroticism. These results suggest that somatic complaints are moderately heritable and that a considerable portion of the covariance between neuroticism and complaints measures is due to genetic factors. Yet, the findings also suggest that these two attributes are distinct entities with overlapping, but not identical, underlying genetic and environmental influences.

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

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.

Dental anxiety in relation to neuroticism and pain sensitivity. A twin study.

Predisposing personality traits as well as heightened pain sensitivity and fear of pain have been hypothesized as central factors in the development of dental anxiety. The aim of the study was to estimate the heritability of dental anxiety, and to investigate the genetic and environmental sources of covariance between dental anxiety on one hand, and pain sensitivity and the neuroticism trait on the other. A sample comprising 188 twins, aged 23-35 years (53 monozygotic and 39 dizygotic twin pairs, and 4 single twins whose co-twin did not participate), was included in the study. Measures of dental anxiety and personality were obtained using Corah's Dental Anxiety Scale and the NEO Personality Inventory Revised, respectively. Heat pain and cold pressor pain sensitivity were assessed using standard pain testing procedures. Bivariate Cholesky models were employed to decompose the correlations between phenotypes into genetic and environmental factors. Using models with common additive genetic (A) and individual-specific environmental (E) factors, moderate heritability (i.e., .41) for dental anxiety was demonstrated. Virtually all of the phenotypic correlation between neuroticism and dental anxiety could be accounted for by A. Furthermore, a substantial part of the variance in dental anxiety was due to specific genetic and individual environmental influences unrelated to neuroticism. The phenotypic correlations between dental anxiety and the pain sensitivity indices were close to zero. Thus, while neuroticism and dental anxiety share a sizeable proportion of genetic (but not environmental) risk factors, the results also suggest that these two attributes are distinct entities with overlapping, but not identical, etiologies.

Psychophysiological responses to pain stimulation and cognitive tasks in female temporomandibular disorder patients.

Background and purpose Psychophysiological factors may contribute to the development of temporomandibular disorders (TMD). Both local orofacial and systemic responses have been investigated. However, most studies have concentrated on physiological responding during cognitive challenges, while responses during painful tasks may be highly relevant for the development of chronic pain conditions. Moreover, the relationship between experimental challenges and physiological responding may be influenced by affective responses during the experimental tasks, an issue not often considered in the literature. Methods This study compared electromyography (EMG) of the left masseter and left trapezius muscles, orofacial and digital skin blood-flow (SBF), mean arterial pressure (MAP), and heart rate (HR) at rest, during orofacial isometric contraction, electrocutaneous pain stimulation of the left hand, pressure pain stimulation of the masseter muscle and the sternum, and three cognitive tasks (reading aloud, a simulated job interview, and visuomotoric tracking). The participants were 25 TMD patients and 25 matched pain-free controls, all females. Affective responses were assessed with the State part of the State-Trait Personality Inventory and with Visual Analogue Scales. Results Masseter EMG levels were significantly lower in the TMD group relative to the control group during jaw contraction, pressure pain stimulation, the relaxation periods, and cognitive tasks. SBF, MAP, and HR responses were largely similar in the two groups, with SBF responses to pain stimulation evident at lower levels of stimulation than previously found. The TMD patients reported significantly higher levels of negative affect during the experiment. Conclusions and implications The low EMG responses in the TMD group may be taken in support of the Pain Adaptation Model of musculoskeletal pain, in which reduced muscular activity serves to protect a painful area. However, it may also be supportive of the Integrated Pain Adaptation Model, where higher central nervous structures influence local muscular output. The group similarities in systemic physiological responding in combination with the elevated levels of negative state affect in the TMD patients confirm previous reports of psychosocial differences being more reliable indicators of TMD than generalized physiological responding.

Experimental pain sensitivity in women with temporomandibular disorders and pain-free controls: the relationship to orofacial muscular contraction and cardiovascular responses.

OBJECTIVE: Chronic pain may result both from a generalized hypersensitivity to acute pain, suggestive of central sensitization processes, and dysfunction of the endogenous pain regulatory system. One purpose of this study was to compare experimental pain sensitivity at several anatomic sites in temporomandibular disorder (TMD) patients and pain-free controls during baseline and after standardized mechanical load of the orofacial region. A second purpose was to compare the pain-modulating effects of cardiovascular responses in TMD patients and pain-free controls. METHODS: Experimental pain was induced by electrocutaneous stimulation of the dorsal left hand and pressure algometry at the right masseter muscle and the sternum. The pain sensitivity of the orofacial region was manipulated by isometric contraction of the masseter muscles. Elevations of mean arterial pressure and heart rate were induced by a simulated job interview. RESULTS: At baseline, the TMD patients exhibited a significantly higher electrocutaneous pain threshold. Relative to the healthy controls, the TMD patients reported increased electrocutaneous and pressure pain sensitivity after isometric contraction of the orofacial region. In addition, there were correlations between mean arterial pressure and pain sensitivity in the TMD group only. DISCUSSION: Significant increases in generalized pain sensitivity occurred in the TMD group, but not in the control group, after isometric contraction of the orofacial muscles, suggestive of a central sensitization process in TMD. Moreover, only in the TMD group there were significant associations between cardiovascular responsesand pain sensitivity, challenging previous assumptions of this relationship occurring mainly in pain-free individuals.

Individual differences in pain sensitivity: genetic and environmental contributions.

Large individual differences in pain sensitivity present a challenge for medical diagnosis and may be of importance for the development of chronic pain. Variance in pain sensitivity is partially mediated by genetic factors, but the extent of this contribution is uncertain. We examined cold-pressor pain and contact heat pain in 53 identical (MZ) and 39 fraternal (DZ) twin pairs, and 4 single twins to determine the heritability of the two phenotypes, and the extent to which the same genetic and environmental factors affect both pain modalities. An estimated 60% of the variance in cold-pressor pain and 26% of the variance in heat pain was genetically mediated. Genetic and environmental factors were only moderately correlated across pain modalities. Genetic factors common to both modalities explained 7% of the variance in cold-pressor and 3% of the variance in heat pain. Environmental factors common to both modalities explained 5% of variance in cold-pressor and 8% of the variance in heat pain. The remaining variance was due to factors that were specific to each pain modality. These findings demonstrate that cold-pressor pain and contact heat pain are mainly distinct phenomena from both a genetic and an environmental standpoint. This may partly explain disparate results in genetic association studies and argues for caution in generalizing genetic findings from one pain modality to another. It also indicates that differences in pain scale usage account for a minor portion of the variance, providing strong support for the validity of subjective pain ratings as measures of experienced pain.

Characterizing individual differences in heat-pain sensitivity.

Heat induced pain has been shown to follow a positively accelerating power function for groups of subjects, yet the extent to which this applies to individual subjects is unknown. Statistical methods were developed for assessing the goodness of fit and reliability of the power function for data from individual subjects with the aim of using such functions for characterizing individual differences in heat-pain sensitivity. 175 subjects rated ascending and random series of contact heat stimuli with visual analogue scales for pain intensity (VAS-I) and unpleasantness (VAS-A). Curve fitting showed excellent model fit. Substitution of model estimates in place of observed VAS scores produced minimal bias in group means, about 0.3 VAS units in the ascending series and 1.0 in the random series, on a 0-100 scale. Individual power function exponents were considerably higher for the ascending than for the random series and somewhat higher for VAS-A than for VAS-I (means: ascending VAS-I=9.04, VAS-A=9.80; random VAS-I=4.95, VAS-A=5.67). The reliability of VAS estimates was high (>==.93), and for the ascending series it remained so when extrapolating 4 degrees C beyond the empirical range. Exponent reliability was high for the ascending series (VAS-I=.92; VAS-A=.91), but considerably lower for the random series (VAS-I=.69; VAS-A=.71). Individual differences constituted 60% of the total variance in pain ratings, whereas stimulus temperature accounted for only 40%. This finding underscores the importance of taking individual differences into account when performing pain studies.