Startseite New evidence for a pain personality? A critical review of the last 120 years of pain and personality
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New evidence for a pain personality? A critical review of the last 120 years of pain and personality

  • Brooke Naylor , Simon Boag und Sylvia Maria Gustin EMAIL logo
Veröffentlicht/Copyright: 1. Oktober 2017
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Scandinavian Journal of Pain
Aus der Zeitschrift Scandinavian Journal of Pain Band 17 Heft 1

Abstract

Background

Personality traits may influence development and adjustment to ongoing pain. Over the past 120 years, there has been considerable research into the relationship between pain and personality. This paper presents new evidence for common personality traits found amongst chronic pain sufferers. In particular, it evaluates evidence for Cloninger’s biopsychosocial model of personality in distinguishing typical personality features of chronic pain sufferers. It evaluates this evidence in the context of the past 120 years of research including psychodynamic formulations, MMPI studies, personality disorder investigations, and the influence of neuroticism on chronic pain.

Methods

A literature search was conducted using PubMed, Medline, PsyclNFO, SCOPUS and Cochrane library. Search terms included chronic pain, pain, personality, neuroticism, harm avoidance, self-directedness, attachment, Temperament and Character Inventory (TCI-R), MMPI, MMPI-2, NEO-PI, EPI, Millon Clinical Multiaxial Inventory, Millon Behavioral Health Inventory, Millon Behavioral Medicine Diagnostic, the Personality Assessment Inventory, the Locus of Control Construct and different combinations of these terms.

Conclusions

Recent descriptive studies using Cloninger’s Temperament and Character Inventory (TCI-R) suggest that higher harm avoidance and lower self-directedness may be the most distinguishing personality features of chronic pain sufferers. High harm avoidance refers to a tendency to be fearful, pessimistic, sensitive to criticism, and requiring high levels of re-assurance. Low self-directedness often manifests as difficulty with defining and setting meaningful goals, low motivation, and problems with adaptive coping. Evidence for this personality profile is found across a wide variety of chronic pain conditions including fibromyalgia, headache and migraine, temporomandibular disorder, trigeminal neuropathy, musculo-skeletal disorders and heterogeneous pain groups. Limitations are also discussed. For example, high harm avoidance is also found in those suffering anxiety and depression. While many studies control for such factors, some do not and thus future research should address such confounds carefully. The evidence is also evaluated within the context of past research into the existence of ‘a pain personality’. Psychodynamic formulations are found to be deficient in objective scientific methods. MMPI studies lack sufficient evidence to support ‘a pain personality’ and may be confounded by somatic items in the instrument. More recent neuroticism studies suggest a relationship between neuroticism and pain, particularly for adjustment to chronic pain. Personality disorders are more prevalent in chronic pain populations than non-pain samples.

Clinical implications

Because harm avoidance reflects a tendency to developed conditioned fear responses, we suggest that higher harm avoidance may create more vulnerability to developing a fear-avoidance response to chronic pain. Furthermore, lower self-directedness may contribute to keeping a sufferer within this vicious cycle of fear, avoidance and suffering. Moreover, we suggest that harm avoidance and self-directedness are broader and more complex constructs than current clinical targets of CBT such as fear-avoidance and self-efficacy. Thus, assessing such personality traits may help to address the complexity of chronic pain presentations. For example, it may help to identify and treat sufferers more resistant to treatment, more prone to comorbidity and more vulnerable to entering the vicious cycle of chronic pain, suffering and disability.

Keywords: Chronic pain; Personality; Harm avoidance; Self-directedness; Neuroticism

1 Introduction

Reflections from Karen,[1] a chronic pain sufferer:

“I often get told that I’ve changed since I developed chronic pain. It makes me really sad. I’m afraid that the pain will never go away. I don’t want to visit my friends anymore. It’s so depressing when you visit friends with so much pain – I can’t laugh when they’re all laughing. Yes, I think my friends are right. I’m a different person to who I was before I had pain. My husband says that I might even have developed it because I’ve always been such a fearful person. I wonder if it might actually be part of my personality, and I’m afraid that it will never go away”.

Chronic pain is a complex phenomenon, generally recognised as involving psychological as well as physical dimensions. Specifically, it is conceptualised as multidimensional with not only sensory but also cognitive, affective, and social components [1]. Evidence is arising that people with different chronic pain types (neuropathic, nociceptive and inflammatory) share similar pain experiences of affective-motivational, cognitive-evaluative and social components, despite sensory-discriminative differences [2,3,4]. Therefore, if there are common psychosocial states associated with chronic pain, independent of chronic pain type, could there also be typical personality traits underlying chronic pain? Indeed, many clinicians note anecdotally that chronic pain sufferers often present with personality and interpersonal issues [5]. Research findings also suggest that chronic pain sufferers display elevated levels of anxiety and depression [6] and personality disorders [7].

Personality traits are ‘enduring patterns of perceiving, relating to, and thinking about the environment and oneself that are displayed in a wide range of social and personal contexts’ [8]. Personality traits may be important to the understanding and treatment of chronic pain, as they maybe implicated in the development and adjustment to chronic pain [9,10]. While older studies could not confirm a typical pain personality, new evidence suggests that a pain personality independent of chronic pain type may exist.

2 Purpose and overview

This paper presents new evidence for common personality traits found amongst chronic pain sufferers. In particular, it evaluates Cloninger’s model of higher harm avoidance and lower self-directedness as distinguishing personality features of chronic pain. It evaluates this new evidence in the context of the past 120 years of research into the question of the relationship between personality and pain. Moreover, potential clinical implications of these personality traits for chronic pain development and maintenance will be suggested.

3 Methods

A literature search for this critical review was conducted using PubMed, Medline, PsycINFO, SCOPUS and Cochrane library. Search terms included chronic pain, pain, personality, neuroticism, harm avoidance, self-directedness, attachment, Temperament and Character Inventory (TCI-R), MMPI, MMPI-2, NEO-PI, EPI, Millon Clinical Multiaxial Inventory, Millon Behavioral Health Inventory, Millon Behavioral Medicine Diagnostic, the Personality Assessment Inventory, the Locus of Control Construct and different combinations of these terms.

4 History of the relationship between pain and personality

While this paper focusses on the last 120 years, it is interesting to note that the link between personality and pain has been explored throughout the ages [11]. For example, during the stone age, Chinese medicine conceptualised pain as arising from problems with blood flow and ‘qi’ caused by imbalances between the physical and intra-personal opposites of yin and yang [12]. During the classical period, the ancient Greek physician Hippocrates proposed one of the first theories of personality by positing that four internal bodily fluids, or ‘humours’ were responsible for personality temperaments as well as specific physical and mental disorders. He believed that pain was due to an imbalance in one of these ‘humours’, which included blood, black bile, yellow bile and phlegm. Other Greek philosophers such as Plato and Aristotle believed that pain arose not only from physical stimuli but also from emotions in the soul and heart [13]. These ideas about pain and personality highlight the ancient holistic mind-body tradition that is now reflected in the modern biopsychosocial model of medicine.

4.1 The psychodynamic approach

Since the 19th century, the link between personality factors and the pain experience has been explored, often due to the failure of the biomedical model of health to explain persistent pain without clear biological cause [14]. This is because the biomedical model of health focussed purely on biological factors and excluded psychological, environmental and social influences [10].

Early research focussed on personality as a causal factor for chronic pain. For example, the psychodynamic theorists, led by Freud, posited a conversion model of pain, whereby the sufferer ‘converted’ emotional pain to somatic symptoms due to underlying personality and emotional conflicts [15]. This basic premise influenced later psychoanalytical theorists such as Engel [16], who proposed the notion of a ‘pain-prone’ patient. Engel posited a ‘psychogenic pain’ theory to explain pain without apparent physical cause. According to Engel, early and lifelong associations with pain caused some individuals to use pain unconsciously to resolve conflicts and maintain emotional equilibrium. He suggested that from birth, a child built a ‘library’ of emotional associations with physical pain and that later these associations could be triggered without actual physical pain. For example, if a child experiences pain and cries, and is subsequently comforted by her mother, the pain becomes a cue for reunification with a love-object. Engel also suggested that this early conditioning developed into a ‘pain prone personality’ which was characterised by feelings of guilt, suffering, defeat, strong unfulfilled aggressive drives and loss, or fear of loss in relationships.

Building on these ideas, Blumer and Heilbronn posited a ‘pain-prone disorder’ which they characterised as a variant of’depressive disease’ for patients without clear organic cause for their pain [17]. They described these patients as expressing continuous pain complaints, having a pre-occupation with somatic symptoms, and displaying inactivity, anhedonia, alexithymia, despair and insomnia. Blumer and Heilbronn suggested that many of these symptoms were simply ‘masked depression’ and that sufferers transformed their depressive pain into physical pain as a means of coping with inner feelings of guilt, neediness and conflict about owning such feelings.

These psychodynamic perspectives were important because they suggested that psychological and personality factors played a role in chronic pain. However, the evidence for a ‘pain-prone patient’ was criticised as being unconvincing, based on anecdotal accounts, and possessing rudimentary scientific methods [18,19].

4.2 The trait theoretical approach

In direct contrast to rudimentary methods of the psychodynamic approach, trait theorists from the 1950s onwards attempted to find objective and scientifically measurable, personality traits in chronic pain sufferers. For this purpose, a variety of psychometric instruments were used including the Personality Assessment Inventory (PAI), the Millon Multiaxial and Health Inventories, the Locus of Control Construct, the Minnesota Multiphasic Personality Inventory (MMPI), the Eysenck Personality Inventory (EPI) and the Neuroticism, Extroversion and Openness Personality Inventory (NEO-PI) among others. While some inventories may be useful, particularly in predicting the patient coping styles which respond better to treatment, this review will focus primarily on MMPI, EPI and NEO-PI studies, as this research more directly addresses the question of a chronic pain personality profile. The MMPI was designed to assess psychopathology in clinical populations and the NEO-PI and EPI to measure non-clinical groups. Most studies focussed on a trait related to emotional reactivity and a tendency towards negative emotional states, although used different labels. For example, the MMPI labels this as ‘hypochondriasis, depression and hysteria’ whereas The EPI and NEO-PI using the term ‘neuroticism’.

4.2.1 MMPI descriptive studies

Early MMPI research tried to discriminate psychological from physical causes of chronic pain by identifying personality traits common to these different groups of sufferers [5]. For example, Hanvik [20] identified clinical elevations among a large number of chronic pain sufferers without a diagnosed physical cause on MMPI scales one to three. These scales measured hypochondriasis, depression and hysteria respectively. The scoring for depression tended to be slightly lower than hypochondriasis and hysteria, so this pattern was labelled the ‘conversion V’ pattern, or ‘neurotic triad’ due to its visual ‘V’ impression. These results were interpreted as support for the psychodynamic formulation of pain, whereby depressed individuals, unable to express their emotions, convert them into physical symptoms. A number of studies found support for a conversion ‘V’ pattern of scoring in a large group of chronic pain sufferers [21,22]; however, many researchers reported only the mean MMPI profile, perhaps over-interpreting these sufferers as one homogenous group [23]. Moreover, other studies found evidence of more than one personality profile of chronic pain sufferers using the MMPI [24,25,26,27,28]. This research raised questions about whether the conversion ‘V’ personality pattern on the MMPI was common for all chronic pain patients or whether there were subgroups of personality types.

One theorist to investigate the question of subgroups was Sternbach [28,29,30] who identified four common patterns of MMPI scoring for chronic pain sufferers, including the ‘conversion V’. The first group displayed clinical elevations on the scales for hysteria and hypochondriasis and were characterised as preoccupied with somatic concerns. The second group was labelled an ‘emotionally overwhelmed’ type, and displayed elevations on all of the first three subscales. Sternbach [29] concluded that these individuals suffered from depression and anxiety, perhaps due to somatic pain and were most responsive to treatment. The third subgroup displayed the conversion ‘V’ pattern, and the fourth subgroup displayed elevations on scale four, ‘psychopathic deviance’, as well as scales one to three. These patients were described as angry, manipulative and ‘acting out’ by using physical symptoms to get needs met. Sternbach [28] suggested that chronic pain sufferers suffered commonly from depression and a variety of neurotic disturbances characterised by pre-occupations with somatic symptoms.

Several other descriptive studies tried to replicate Sternbach’s MMPI sub-group findings. The ‘emotionally overwhelmed type’ and ‘conversion V’ were upheld, although other subgroups were not replicated [24,25,27]. Therefore, MMPI descriptive studies did not offer any consistent evidence of one chronic pain personality; rather, they suggested that there may be subgroups of personality profiles for some chronic pain sufferers [5].

4.2.2 MMPI prospective studies

Another approach to examining the relationship between pain and personality is to examine whether personality features are causal in the development of chronic pain. A small set of studies did this using prospective study designs. These studies attempted to tease out this relationship, by measuring the personality of healthy individuals with the MMPI and tracking the development of chronic pain over time [31,32,33,34]. One study [31] following 400 Danish men and women over 20 years found some support for greater incidence of pain in those scoring higher on hypochondriasis, hysteria and depression scales before pain onset. Another which tracked 3000 Boeing employees over four years found that those scoring in the upper quintile on the hysteria scale were more likely to develop lower back pain [34]. These studies, as well as producing inconsistent findings, also suffered from methodological flaws. For example, in one study [31], the physical status of participants was not recorded. Therefore, it was not possible to determine if higher MMPI scores were the result of an understandable focus on greater physical symptoms [31]. Moreover, adding to the complexity, other factors were also strong predictors of pain development such as gender, job dissatisfaction [34], filing of workers compensation claims, and initial scores on pain and disability measures [33].

In summary, evidence from MMPI studies between 1950 and 2000, appeared to support the notion of different MMPI personality profiles among varied chronic pain types. However, there was insufficient evidence to support a ‘pain-prone personality’, even though there was some evidence that a large proportion of chronic pain sufferers experienced emotional problems [6]. Many studies also had methodological flaws such as lack of control groups and confounding variables [14]. For example, the MMPI was criticised because many items use somatic symptoms to assess underlying neurotic traits [14,35]. Therefore, chronic pain sufferers may be responding more to physical symptoms of pain rather than to underlying neurotic problems. As a result, since the 1990s, there has been a dramatic decline in MMPI investigations of chronic pain populations [36], although the improved MMPI-2-has still been used to a lesser extent and the revised MMPI-2-RF was validated in a low back pain population recently [36].

4.2.3 Neuroticism and descriptive studies

Another line of inquiry from the trait perspective involves the role of non-pathological factors, namely the trait dimension ‘neu-roticism’, as measured by scales such as the NEO-PI [37] and EPI [38] (Eysenck Personality Inventory) and its relationship to chronic pain. Neuroticism reflects a person’s tendency to experience negative emotions such as anger, anxiety, irritability, depression and low self-esteem. Those high in neuroticism are more emotionally reactive and vulnerable to stress. They are also more likely to interpret ordinary situations as threatening and minor frustrations as hopelessly difficult. While the term neuroticism is problematic as it may seem pejorative for the layperson due to its common association with emotional instability and reactivity, it will be used in this review because this is the term used in the research. However, the authors note that neuroticism is a normal personality dimension that varies between individuals.

It is suggested that neuroticism is linked to a range of physical illnesses including chronic pain [39]. As a result, a number of descriptive studies have assessed if chronic pain sufferers display higher levels of neuroticism compared to control groups. A considerable number of studies have found this to be the case in various chronic pain types [40,41,42,43,44,45,46,47,48,49]. However, other studies have found relatively normal personality profiles, or only sub-groups of chronic pain sufferers with higher neuroticism [50,51,52,5354]. Unfortunately, many studies, particularly the older ones, suffer from the similar methodological flaws and lack of scientific methods found in early MMPI studies. As a result, evidence is inconclusive. Despite this, some recent studies supporting increased neuroticism present some interesting evidence due to larger, more representative samples, healthy control groups and sounder methods [45,55]. However, larger, more controlled studies are needed.

4.2.4 Neuroticism and prospective studies

Others have suggested that neuroticism may be a causal factor for chronic pain. Several theorists [39,56,57,58] have suggested that neuroticism is causally related to physical illness including chronic pain because it creates a greater physiological response to stress, which may contribute to changes associated with disease states. Another argument suggests that neuroticism pre-disposes individuals to lifestyle factors which may increase the risk of disease [59,60].

Several studies have tested this aetiological link using prospective study designs where a group of healthy individuals is tracked over time for pain development. For example, Pietri-Taleb et al. [61] followed 1015 machine operators, carpenters and office workers over three years. Higher neuroticism scores predicted the development of ‘severe neck trouble’ in the machine operator group. Similar results were found for headache in a group of 3676 adolescents [62] and migraine [56] among 972 female health workers However, these findings need to be interpreted with caution due to a small number of studies and lack of consistency in how pain was defined.

4.2.5 Neuroticism and adjustment to chronic pain

In contrast to the causal explanation of neuroticism’s role in chronic pain, since the 1980s, much research has focussed on neuroticism as a moderator of the pain experience [6]. The suggestion is that individuals with higher trait neuroticism may respond more poorly to pain than those with lower neuroticism, and as a result may be more likely to suffer more and exacerbate the pain experience. Because of this maladjustment, in terms of a ‘pain-personality’, heightened neuroticism may be one personality trait which leads acute pain to develop into chronic pain, or it may be one personality characteristics which develops after onset of chronic pain and compounds adjustment. Several mechanisms have been suggested to explain the influence of neuroticism on adjustment.

The first suggested mechanism is that neuroticism may create heightened physical sensitivity to pain due to its inherent connection with chronically moderated anxiety [47,63,64,65,66,67]. As a result, sufferers may be more likely to attend to their pain and bodily symptoms, thus leading to hypervigilance and amplification of symptoms, which are suggested cognitive-affective components in the development of chronic pain [68]. However, there are mixed results for reported pain intensity in chronic pain sufferers, with some studies finding higher reported pain intensity for more neurotic subjects and others finding no connection [69,70,71].

Another suggested mechanism is that neuroticism influences adjustment to pain by affecting pain-related beliefs and emotional distress. For example, Harkins et al. [71] investigated the relationship between neuroticism as measured by the EPI, and experimental and clinical pain intensity. When subjected to the same intensity of noxious stimulus, those with higher neuroticism scores reported greater emotional distress. In addition, Wade et al. [70] reported a relationship between neuroticism, heightened emotional distress and negative pain-related beliefs such as the ability to endure pain, reduce pain and confidence that the pain will be cured. Other studies have found similar results [69,72]. Limitations of some studies include a lack of psychometric properties for emotion and cognition measures, small sample sizes, and statistical problems. However, two methodologically sound longitudinal studies with rheumatoid arthritis sufferers also reported similar associations between neuroticism and negative mood in chronic pain sufferers [73].

The third suggested mechanism is that neuroticism leads to less-adaptive and passive coping strategies. Several studies have found a relationship between this trait and maladaptive coping skills including: relinquishing control over pain to another person; allowing pain to adversely affect other areas of life; less effective problem-solving; fewer cognitive restructuring strategies; greater use of emotional expression and fewer relaxation activities [44,74,75,76].

4.2.6 Neuroticism and the fear avoidance model of chronic pain

Another recent line of research has focussed on the link between neuroticism and components of the fear avoidance model of chronic pain. This model suggests that personality vulnerabilities may lead certain people to be more threatened by pain, thus resulting in greater pain-related fear, avoidance and disability [9]. Catastrophizing is a ruminative thinking style which tends to exaggerate negative responses to potential or actual pain. It is conceptualised as a pre-cursor to pain-related fear and avoidance and has been linked to more severe pain, psychological distress, impaired coping and increased disability [77]. Several studies have found that neuroticism may contribute to greater catastrophizing about pain [73,78]. Others have found that neuroticism indirectly affects pain-related anxiety through its influence on catastrophizing [42,77]. Goubert et al. [79] also found that neuroticism and vigilance to pain were related to pain catastrophizing and fear of movement re-injury. However, not all studies have found a relationship between neuroticism and catastrophizing [69].

Finally, anxiety sensitivity and injury/illness sensitivity, lower-order constructs of neuroticism and trait anxiety, have also been implicated in the fear avoidance model. Anxiety sensitivity refers to the tendency to react anxiously to one’s own anxiety and anxiety-related physical sensations. Injury/illness sensitivity refers to ‘fearfulness of imminent injury and illness’ [80]. A number of studies have found anxiety sensitivity to be positively correlated with pain-related anxiety among healthy [81] and chronic pain samples [82]. Higher anxiety sensitivity has also been found to be indirectly related to higher avoidance [83]. In a study by Vancleef et al. [80], injury/illness sensitivity was found to be more predictive of fear of pain, pain catastrophizing and anticipatory fear than anxiety sensitivity.

4.2.7 Summary

In summary, there is some evidence to suggest a relationship between neuroticism and chronic pain. Sufferers may display moderately higher levels of neuroticism than pain-free individuals. In addition, neuroticism may affect adjustment to ongoing pain, increasing suffering and disability, and potentially contributing to the development of chronic pain. However, many of the studies do not control for anxiety and depression which may be confounding variables when measuring neuroticism. Moreover, neuroticism represents only one trait while most models of personality functioning such as the MMPI, five-factor model and temperament and character inventory include multiple personality dimensions. Therefore, neuroticism in and of itself cannot represent a pain personality type – either for a sub-group or a greater whole of chronic pain sufferers.

4.3 Studies investigating personality disorders and attachment

While the trait theorists focussed on personality profiles from empirical personality questionnaires, another approach since the 1980s has examined personality disorders in the chronic pain population through structured and semi-structured clinical interviews. Compared to rates in the general and even psychiatric population, the prevalence of personality disorders in chronic pain populations is higher, ranging from 31% to 59% [5]. While some have argued that certain personality disorders may pre-dispose individuals to develop chronic pain [84], others have suggested that a stress-diathesis model may explain the higher incidence of personality disorders in the chronic pain population. While the Diagnostic and Statistical Manual of Mental Disorders-5 [8] suggests that personality disorders represent ‘a longstanding and life-long pattern of internal and external behaviours’, the stress-diathesis model posits that an acute stressor such as ongoing pain may exacerbate underlying personality vulnerabilities, and if not adequately managed, result in a personality disorder. There is growing support for the stress-diathesis model of chronic pain and personality disorders [85,86].

Another approach which has conceptualised chronic pain as a stressor for the onset of personality difficulties is the attachment-diathesis model of chronic pain [87]. This model suggests that insecure attachment is a risk factor for development of chronic pain and a vulnerability factor for poorer outcome and disability. Evidence from several studies suggests that insecure attachment is linked to psychosocial variables such as heightened threat perceptions around pain, less adaptive coping and more negative perceptions of available social support. According to the model, these psychosocial variables may affect onset, maintenance and adjustment to chronic pain.

These stress-diathesis models raise important questions about the causality of personality and pain. Do particular personality characteristics lead to chronic pain or does the onset of chronic pain trigger personality dysfunction? Or perhaps, there is a dynamic interaction between the two. Others have suggested that this question is more complex than just bidirectional causality. For example, Fernandez and Kerns suggest affective disturbance and pain may be framed in terms of predisposing, precipitative, perpetuating and exacerbating factors as well as consequences [88].

This issue of causality has also been raised as an issue of personality measurement given that there is now strong evidence that state factors (such as chronic pain) may influence or distort trait measurement [89]. Therefore, it cannot be assumed that personality measurement after chronic pain onset reflects a stable pre-pain personality. This has implications for many studies (including the ones in this review) which measure personality after onset. However, regardless of causality, the stress-diathesis model of chronic pain and personality may still be compatible with a common personality profile, as perhaps the exacerbation of trait vulnerabilities, including those that maybe more prominent in chronic pain, is due to changes brought on by pain itself. However, further investigation into the nature and direction of causality is needed.

In summary, it appears that personality disorders are more prevalent in the chronic pain population. Insecure attachment may also be a contributing factor to personality and psychosocial difficulties in the pain context. There is much anecdotal evidence from clinicians about personality difficulties amongst chronic pain patients such as heightened dependency, anxiety and aggression. However, because much past evidence has been inconclusive, new frameworks are required to assess this relationship and provide more explanatory power.

5 New evidence for a pain personality

5.1 The Temperament and Character Inventory (TCI-R)

In line with the biopsychosocial approach to chronic pain, Robert Cloninger, a molecular biologist and psychiatrist, published the Temperament and Character inventory in 1994 [90]. Cloninger divides personality into 4 temperament and 3 character dimensions, with temperament reflecting genetically determined personality characteristics and character reflecting traits affected by learning. Temperament traits include: harm avoidance; reward dependence; novelty seeking and persistence. Character traits include: self-directedness; cooperativeness and self-transcendence. The temperament dimensions manifest as automatic emotional responses to experience and reflect neurotransmitter systems in the brain. Harm avoidance is linked to serotonin, reward dependence is linked to noradrenalin, and novelty seeking is linked to dopamine. In contrast, character dimensions reflect cognitive self-concepts and individual differences in goals and values which influence the choices and meanings of life experience. Cloninger suggests that character dimensions are affected by the environment and experience, and that character matures until late adulthood.

The TCI-R differs from other personality inventories such as the MMPI and NEO-PI, because it suggests that genetic and environmental factors influence personality development differently [90]. Changes in personality and manifestations of personality dysfunction are mainly suggested by the character domain because these can be affected by learning, although temperament, which is biologically determined, may influence the type of personality problem. The TCI-R may also be particularly relevant to chronic pain because serotonin, the neurotransmitter related to harm avoidance, is implicated in the inhibition of pain in the central nervous system [91,92].

5.2 A personality profile of higher harm avoidance and lower self-directedness

A new line of evidence suggests that the TCI-R may identify a personality profile common to chronic pain sufferers. A number of studies have found significantly higher harm avoidance (HA) and lower self-directedness (SD) compared to healthy controls and normative samples in chronic pain sufferers. People with high HA are often described as being worrying and fearful, sensitive to criticism and punishment, and pessimistic even in situations that do not worry other people. They are more likely to develop conditioned fear responses and require more reassurance and encouragement. Individuals low in SD are often described as blaming, destructive, fragile and lacking an internal locus of control, which prevents them from setting and meeting meaningful goals. They also tend to have low self-efficacy which further impacts motivational states and self-esteem.

This profile is found in studies reflecting a range of pain types such as fibromyalgia [93,94,95,96], migraine and chronic tension type headache [97,98,99], non-specific musculo-skeletal disorders [100], as well as temporomandibular disorder, trigeminal neuropathy and heterogeneous chronic pain groups [101,102,103,104].

For example, in a controlled study, Conrad et al. [102] administered the TCI-R to 207 heterogeneous chronic pain sufferers and 105 pain-free controls and found that the chronic pain group displayed higher levels of HA and lower SD and Co-operativeness (CO), even after controlling for anxiety and depression. Malmgren-Olsson and Bergdahl [100] also found similar results when they compared 78 sufferers with musculo-skeletal pain and 118 healthy controls. They also found that HA and SD correlated with depression and anxiety symptoms. Given the high comorbidity of mood and anxiety disorders in chronic pain, the authors suggested that the profile of higher HA and lower SD may suggest a ‘mood and pain prone personality type’.

In addition, Mazza et al. [93] administered the TCI-R to 60 fibromyalgia sufferers and 80 healthy controls before and after a 6-month SSRI treatment. They found higher levels of HA and lower levels of SD before treatment in the pain group. After treatment, HA scores were reduced and SD scores were increased, and both remained significantly different from the control group. When depression symptoms were added as a covariate, HA was still significantly higher than controls, and SD no longer achieved significance. This suggests that SD may be more state dependent than HA, in line with Cloninger’s theory.

Gustin et al. [101] further explored a ‘mutual pain personality’ by comparing patients with temporomandibular disorder (nociceptive pain) and trigeminal neuropathy (neuropathic pain). They found that both groups had significantly higher HA and lower SD compared to a healthy control group. The authors suggested that this was significant because previous studies had only compared single chronic pain diagnoses such as headache and migraine, whereas this study compared the two broad categories of chronic pain: neuropathic and nociceptive pain, while also controlling for pain site. Therefore, a similar personality profile of higher HA and lower SD in these two different pain groups may suggest ‘a mutual personality profile’ in chronic pain sufferers in general. Indeed after evaluating the evidence in his review paper, and noting that the majority of studies found this TCI-R personality profile, Conrad et al. [92] suggested that higher HA and lower SD may be the most distinguishing personality feature of chronic pain sufferers thus far in the research.

Furthermore, several studies also suggest that higher HA and lower SD may be associated with Cluster C or ‘fearful’ personality disorders, such as avoidant, obsessive-compulsive and dependent personality disorders [96,102,105,106]. For example, Garcia-Fontanals et al. [96] found alongside a profile of higher HA and lower SD for chronic pain sufferers, that nearly one third met the DSM criteria for a Cluster C personality disorder. Conrad et al. [102] found that 27% of chronic pain patients met criteria for Cluster C personality disorders.

While the results of these studies display promising findings, some limitations of the research should be noted. Firstly, while a majority of studies have found a profile of higher HA and lower SD in chronic pain sufferers, not all have done so [107,108]. Secondly, another interesting observation is that higher HA and lower SD may also be found in depression and anxiety sufferers. Indeed HA is conceptualised as a temperamental vulnerability for developing anxiety and depression [90]. Therefore, when measuring the personality of chronic pain sufferers, mood and anxiety symptoms must be carefully controlled to ensure that higher HA and lower SD independently reflect chronic pain, not only state factors. Many of the studies do control for these variables [94,96,100,102,104] and find this profile to reflect chronic pain independent of state factors, although they are often highly correlated. Given the high comorbidity of depression and anxiety with chronic pain, this seems very reasonable. However, not all studies do control for depression and anxiety. Therefore, more controlled studies with larger, more representative samples are needed before firm conclusions can be drawn.

5.3 Summary

In summary, evidence is arising that chronic pain sufferers may display a common personality profile of higher HA and lower SD as measured by Cloninger’s TCI-R. This contrasts with past research which has investigated such a phenomenon and either failed to find empirical evidence, produced inconsistent findings or lacked the personality framework to provide a broader personality profile. The early psychodynamic theorists suggested a conversion personality, whereby depressed individuals converted their emotions into physical symptoms; however, this theory was rejected due to lack of objective methods. MMPI studies found some evidence for an ‘emotionally overwhelmed’ subtype; however this profile was not common to all chronic pain sufferers. Investigations into neuroticism, as measured by the NEO-PI and EPI, have provided more promising results and suggest a modest relationship between neuroticism and chronic pain, particularly in terms of adjustment to pain. This is unsurprising, however, because neuroticism and harm avoidance are overlapping constructs with an estimated correlation of .71 [105]. However, measures such as the NEO and EPI provide perhaps a limited personality profile, as the models include only five traits, of which one is relevant. Therefore, heightened neuroticism may not be broad enough to represent a personality profile. Studies investigating personality with the TCI-R represent a new area of research, as many have replicated a profile of higher HA and lower SD in a broad range of chronic pain types. However, not all have done so, and these personality dimensions are often correlated with state factors, so more controlled studies with larger sample sizes are needed. Nevertheless, the preliminary evidence is promising, and importantly, may be useful for treatment.

Finally, it is also necessary to make a few points about the inherent limitations of personality and chronic pain research as most are cohort studies and thus representative sampling is an issue. In addition, much of the research is cross-sectional and therefore cannot contribute to the question of whether personality traits predispose an individual to chronic pain or whether the personality characteristics emerge after the onset of pain.

Moreover, a profile of higher HA and lower SD, while important to chronic pain may not be exclusive to it, just as elevated neuroticism may be found amongst people with different mental and health disorders [39]. Other conditions known to display this profile include menopause [109], as well as anxiety [110,111], and mood disorders [112,113]. Thus, the trans-diagnostic nature of this personality profile highlights the interconnectedness of physical and mental health problems.

5.4 Clinical implications of higher harm avoidance and lower self-directedness

So, what does a personality profile of higher HA and lower SD mean and how can it help chronic pain treatment? We suggest that assessing for this personality profile may help to conceptualise underlying mechanisms of chronic pain and help treat the complexity of chronic pain presentations.

Firstly, we argue that such a personality profile may be a factor in individuals developing a fear-avoidance response to pain, which contributes to the development and maintenance of chronic pain (Fig. 1). There is growing evidence for the fear avoidance model in the development and maintenance of chronic pain [68,114,115]. This model suggests that certain personality traits may be a vulnerability factor in developing greater fear around pain [9]. We suggest that elevated HA and lower SD may represent such a personality vulnerability which may lower the threshold at which pain is perceived as threatening. As a result, higher HA sufferers may be more likely to anticipate pain with fearful, catastrophic thoughts, which may develop into chronic rumination and worry. In line with the fear avoidance model [9], these negative appraisals may then lead to pain-related fear which results in avoidance of feared movement and activities. Consequently, this avoidance then results in disuse, disability and depression, further exacerbating the pain experience and maintaining a vicious cycle of fear and avoidance, which is often characteristic of chronic pain sufferers.

Fig. 1 Vicious cycle of chronic pain, harm avoidance and self-directedness; HA: harm avoidance, SD: self-directedness.
Fig. 1

Vicious cycle of chronic pain, harm avoidance and self-directedness; HA: harm avoidance, SD: self-directedness.

Lower self-directedness, which is closely related to self-efficacy, may make it more difficult for chronic pain sufferers to prevent and overcome this vicious cycle. This is because they lack the skills to set and achieve meaningful goals and cope actively. Therefore, sufferers scoring lower in SD may find it difficult to stop chronic rumination, to take action to overcome avoidance and to engage in more active coping behaviours.

Therefore, assessing and addressing higher HA and lower SD may be useful for treatment. Research suggests that anxiety related personality traits can be improved with cognitive-behavioural therapy (CBT) [116], and CBT anxiety treatment protocols are suggested to be effective for chronic pain management [117,118]. Cognitive restructuring may help to address catastrophic thinking. Graded exposure and behavioural experiments for feared activities may help to address avoidance and fearful beliefs. For example, a sufferer who fears that ‘bending’ or ‘gardening’ will cause re-injury, can be exposed to such activities in order to disconfirm catastrophic beliefs and reduce fear.

Cognitive behavioural treatments may also be useful in addressing lower self-directedness in individuals. Indeed cognitive behavioural treatment has been found to improve SD [102]. Useful components include goal setting, communication and assertiveness skills, active coping skills and problem solving.

Moreover, high HA is suggested to be a vulnerability factor in developing mood and anxiety disorders [90]. Given the high comorbidity of these disorders with chronic pain, it is possible that there may be a shared vulnerability to developing pain, anxiety and depressive symptoms [119]. Therefore, a transdiagnostic approach may be useful in reducing the emotional suffering and disability linked to chronic pain. Trials of cognitive behaviour therapy which include components for chronic pain, anxiety and depression have produced promising results [120,121].

While CBT treatment for chronic pain creates modest improvements for sufferers, outcomes could be greatly improved. Harm avoidance and self-directedness represent broader and deeper constructs than fear-avoidance and self-efficacy, which are common targets of CBT treatment. HA is broader than fear-avoidance as it not only refers to cognitive-behavioural correlates of fear, it also refers to other personality characteristics which may compound adjustment to chronic pain such as pessimistic thinking, chronic tiredness, fatigue-proneness, the need for reassurance, and sensitivity to criticism and punishment. Similarly, SD is a broader dimension than self-efficacy because it encompasses not only the belief that one can achieve personal goals, but also personality features such as blaming, destructiveness, fragility of character, and a tendency to live a life more influenced by environmental factors than internal values and goals. Therefore, assessing for higher HA and lower SD will enhance case formulation and may signal the need for broader and deeper treatment methods. For example, if a patient is sensitive to criticism or has a strong need for re-assurance, therapies such as schema therapy which focus on the quality of the therapist-client relationship and address attachment needs may engender a greater sense of self and security in the client, a reduced need for re-assurance and thus enhanced resilience. Another target for treatment included in SD is a tendency towards self-destructiveness. For example, drug overuse is a problem in chronic pain populations. Dialectical behaviour therapy strategies such as distress tolerance and emotion regulation skills specifically address such destructive behaviours. There is some evidence to support application of these skills in chronic pain treatment [122].

Thus, assessing HA and SD may help clinicians anticipate clients who are less responsive to treatment, and more vulnerable to co-morbidity and the vicious cycle of chronic pain, suffering and disability.

5.5 Recent developments in personality and neuroscience

A final note on recent developments in neuroscience, plasticity, personality and pain: recent evidence from MRI imaging studies suggests that chronic pain may be linked to subtle changes in brain anatomy, which may result in changes in personality [123]. It is generally accepted that gross damage to certain brain areas such as the prefrontal cortex can result in personality changes; the case of Phineus Gage [124] is a well-known example. However, recent advances in brain imaging techniques make it possible to explore more subtle brain changes, which may also result in alterations in personality. In exploratory research, Gustin et al. [123] found that there are differences in neuronal dendritic length and spine densities in the prefrontal cortex in chronic neuropathic pain sufferers compared to healthy controls. This difference was found in brain areas underpinning personality traits and was correlated with reduced novelty seeking scores as measured by the TCI-R. These results indicated that brain differences may reflect reduced functioning in personality. Another recent study [125] found that lower levels of prefrontal N-acetylaspartate (NAA), a biochemical measure of neuronal integrity [126], were significantly correlated with higher harm avoidance in chronic pain sufferers compared to healthy controls. This indicates that perhaps some of the higher incidence of fear and worry in those with chronic pain is linked to subtle changes in neuronal integrity due to chronic pain itself. Interestingly, the animal model of pain has shown that the pre-frontal cortex is altered after nerve injury, and that this only occurs on the contra-lateral brain side to the injury [127]. This provides evidence that the changes in the prefrontal cortex occur after onset of pain and may result in changes in emotion, personality and cognition. While much more human longitudinal research is needed, these findings strongly support the idea that biochemical and structural changes occur in the prefrontal cortex in chronic pain and that they are also correlated with personality.

Highlights

  • Personality factors are important for understanding chronic pain development and maintenance.

  • Different chronic pain types share a profile of higher harm avoidance and lower self-directedness.

  • This profile helps explain complex presentations and may improve treatment.

  • The past 120 years of research into chronic pain and personality are summarised.

DOI of refers to article: http://dx.doi.org/10.1016/j.sjpain.2017.08.019.

School of Psychology, University of New South Wales, Australia

  1. Funding

    This work was supported by the National Health and Medical Research Council of Australia (GNT1084240) and the Rebecca L. Cooper Medical Research Foundation.

  2. Ethical issues

    Ethic Board approval was not required for this critical review.

  3. Conflicts of interest

    The authors have no conflict of interest to report.

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Received: 2016-12-05
Revised: 2017-07-05
Accepted: 2017-07-05
Published Online: 2017-10-01
Published in Print: 2017-10-01

© 2017 Scandinavian Association for the Study of Pain

Artikel in diesem Heft

  1. Observational study
  2. Perceived sleep deficit is a strong predictor of RLS in multisite pain – A population based study in middle aged females
  3. Clinical pain research
  4. Prospective, double blind, randomized, controlled trial comparing vapocoolant spray versus placebo spray in adults undergoing intravenous cannulation
  5. Clinical pain research
  6. The Functional Barometer — An analysis of a self-assessment questionnaire with ICF-coding regarding functional/activity limitations and quality of life due to pain — Differences in age gender and origin of pain
  7. Clinical pain research
  8. Clinical outcome following anterior arthrodesis in patients with presumed sacroiliac joint pain
  9. Observational study
  10. Chronic disruptive pain in emerging adults with and without chronic health conditions and the moderating role of psychiatric disorders: Evidence from a population-based cross-sectional survey in Canada
  11. Educational case report
  12. Management of patients with pain and severe side effects while on intrathecal morphine therapy: A case study
  13. Clinical pain research
  14. Behavioral inhibition, maladaptive pain cognitions, and function in patients with chronic pain
  15. Observational study
  16. Comparison of patients diagnosed with “complex pain” and “somatoform pain”
  17. Original experimental
  18. Patient perspectives on wait times and the impact on their life: A waiting room survey in a chronic pain clinic
  19. Topical review
  20. New evidence for a pain personality? A critical review of the last 120 years of pain and personality
  21. Clinical pain research
  22. A multi-facet pain survey of psychosocial complaints among patients with long-standing non-malignant pain
  23. Clinical pain research
  24. Pain patients’ experiences of validation and invalidation from physicians before and after multimodal pain rehabilitation: Associations with pain, negative affectivity, and treatment outcome
  25. Observational study
  26. Long-term treatment in chronic noncancer pain: Results of an observational study comparing opioid and nonopioid therapy
  27. Clinical pain research
  28. COMBAT study – Computer based assessment and treatment – A clinical trial evaluating impact of a computerized clinical decision support tool on pain in cancer patients
  29. Original experimental
  30. Quantitative sensory tests fairly reflect immediate effects of oxycodone in chronic low-back pain
  31. Editorial comment
  32. Spatial summation of pain and its meaning to patients
  33. Original experimental
  34. Effects of validating communication on recall during a pain-task in healthy participants
  35. Original experimental
  36. Comparison of spatial summation properties at different body sites
  37. Editorial comment
  38. Behavioural inhibition in the context of pain: Measurement and conceptual issues
  39. Clinical pain research
  40. A randomized study to evaluate the analgesic efficacy of a single dose of the TRPV1 antagonist mavatrep in patients with osteoarthritis
  41. Editorial comment
  42. Quantitative sensory tests (QST) are promising tests for clinical relevance of anti–nociceptive effects of new analgesic treatments
  43. Educational case report
  44. Pregabalin as adjunct in a multimodal pain therapy after traumatic foot amputation — A case report of a 4-year-old girl
  45. Editorial comment
  46. Severe side effects from intrathecal morphine for chronic pain after repeated failed spinal operations
  47. Editorial comment
  48. Opioids in chronic pain – Primum non nocere
  49. Editorial comment
  50. Finally a promising analgesic signal in a long-awaited new class of drugs: TRPV1 antagonist mavatrep in patients with osteoarthritis (OA)
  51. Observational study
  52. The relationship between chronic musculoskeletal pain, anxiety and mindfulness: Adjustments to the Fear-Avoidance Model of Chronic Pain
  53. Clinical pain research
  54. Opioid tapering in patients with prescription opioid use disorder: A retrospective study
  55. Editorial comment
  56. Sleep, widespread pain and restless legs — What is the connection?
  57. Editorial comment
  58. Broadening the fear-avoidance model of chronic pain?
  59. Observational study
  60. Identifying characteristics of the most severely impaired chronic pain patients treated at a specialized inpatient pain clinic
  61. Editorial comment
  62. The burden of central anticholinergic drugs increases pain and cognitive dysfunction. More knowledge about drug-interactions needed
  63. Editorial comment
  64. A case-history illustrates importance of knowledge of drug-interactions when pain-patients are prescribed non-pain drugs for co-morbidities
  65. Editorial comment
  66. Why can multimodal, multidisciplinary pain clinics not help all chronic pain patients?
  67. Topical review
  68. Individual variability in clinical effect and tolerability of opioid analgesics – Importance of drug interactions and pharmacogenetics
  69. Editorial comment
  70. A new treatable chronic pain diagnosis? Flank pain caused by entrapment of posterior cutaneous branch of intercostal nerves, lateral ACNES coined LACNES
  71. Clinical pain research
  72. PhKv a toxin isolated from the spider venom induces antinociception by inhibition of cholinesterase activating cholinergic system
  73. Clinical pain research
  74. Lateral Cutaneous Nerve Entrapment Syndrome (LACNES): A previously unrecognized cause of intractable flank pain
  75. Editorial comment
  76. Towards a structured examination of contextual flexibility in persistent pain
  77. Clinical pain research
  78. Context sensitive regulation of pain and emotion: Development and initial validation of a scale for context insensitive avoidance
  79. Editorial comment
  80. Is the search for a “pain personality” of added value to the Fear-Avoidance-Model (FAM) of chronic pain?
  81. Editorial comment
  82. Importance for patients of feeling accepted and understood by physicians before and after multimodal pain rehabilitation
  83. Editorial comment
  84. A glimpse into a neglected population – Emerging adults
  85. Observational study
  86. Assessment and treatment at a pain clinic: A one-year follow-up of patients with chronic pain
  87. Clinical pain research
  88. Randomized, double-blind, placebo-controlled, dose-escalation study: Investigation of the safety, pharmacokinetics, and antihyperalgesic activity of L-4-chlorokynurenine in healthy volunteers
  89. Clinical pain research
  90. Prevalence and characteristics of chronic pain: Experience of Niger
  91. Observational study
  92. The use of rapid onset fentanyl in children and young people for breakthrough cancer pain
  93. Original experimental
  94. Acid-induced experimental muscle pain and hyperalgesia with single and repeated infusion in human forearm
  95. Original experimental
  96. Swearing as a response to pain: A cross-cultural comparison of British and Japanese participants
  97. Clinical pain research
  98. The cognitive impact of chronic low back pain: Positive effect of multidisciplinary pain therapy
  99. Clinical pain research
  100. Central sensitization associated with low fetal hemoglobin levels in adults with sickle cell anemia
  101. Topical review
  102. Targeting cytokines for treatment of neuropathic pain
  103. Original experimental
  104. What constitutes back pain flare? A cross sectional survey of individuals with low back pain
  105. Original experimental
  106. Coping with pain in intimate situations: Applying the avoidance-endurance model to women with vulvovaginal pain
  107. Clinical pain research
  108. Chronic low back pain and the transdiagnostic process: How do cognitive and emotional dysregulations contribute to the intensity of risk factors and pain?
  109. Original experimental
  110. The impact of the Standard American Diet in rats: Effects on behavior, physiology and recovery from inflammatory injury
  111. Educational case report
  112. Erector spinae plane (ESP) block in the management of post thoracotomy pain syndrome: A case series
  113. Original experimental
  114. Hyperbaric oxygenation alleviates chronic constriction injury (CCI)-induced neuropathic pain and inhibits GABAergic neuron apoptosis in the spinal cord
  115. Observational study
  116. Predictors of chronic neuropathic pain after scoliosis surgery in children
  117. Clinical pain research
  118. Hospitalization due to acute exacerbation of chronic pain: An intervention study in a university hospital
  119. Clinical pain research
  120. A novel miniature, wireless neurostimulator in the management of chronic craniofacial pain: Preliminary results from a prospective pilot study
  121. Clinical pain research
  122. Implicit evaluations and physiological threat responses in people with persistent low back pain and fear of bending
  123. Original experimental
  124. Unpredictable pain timings lead to greater pain when people are highly intolerant of uncertainty
  125. Original experimental
  126. Initial validation of the exercise chronic pain acceptance questionnaire
  127. Clinical pain research
  128. Exploring patient experiences of a pain management centre: A qualitative study
  129. Clinical pain research
  130. Narratives of life with long-term low back pain: A follow up interview study
  131. Observational study
  132. Pain catastrophizing, perceived injustice, and pain intensity impair life satisfaction through differential patterns of physical and psychological disruption
  133. Clinical pain research
  134. Chronic pain disrupts ability to work by interfering with social function: A cross-sectional study
  135. Original experimental
  136. Evaluation of external vibratory stimulation as a treatment for chronic scrotal pain in adult men: A single center open label pilot study
  137. Observational study
  138. Impact of analgesics on executive function and memory in the Alzheimer’s Disease Neuroimaging Initiative Database
  139. Clinical pain research
  140. Visualization of painful inflammation in patients with pain after traumatic ankle sprain using [11C]-D-deprenyl PET/CT
  141. Original experimental
  142. Developing a model for measuring fear of pain in Norwegian samples: The Fear of Pain Questionnaire Norway
  143. Topical review
  144. Psychoneuroimmunological approach to gastrointestinal related pain
  145. Letter to the Editor
  146. Do we need an updated definition of pain?
  147. Narrative review
  148. Is acetaminophen safe in pregnancy?
  149. Book Review
  150. Physical Diagnosis of Pain
  151. Book Review
  152. Advances in Anesthesia
  153. Book Review
  154. Atlas of Pain Management Injection Techniques
  155. Book Review
  156. Sedation: A Guide to Patient Management
  157. Book Review
  158. Basics of Anesthesia
https://doi.org/10.1016/j.sjpain.2017.07.011
Schlagwörter für diesen Artikel
Chronic pain; Personality; Harm avoidance; Self-directedness; Neuroticism

Artikel in diesem Heft

  1. Observational study
  2. Perceived sleep deficit is a strong predictor of RLS in multisite pain – A population based study in middle aged females
  3. Clinical pain research
  4. Prospective, double blind, randomized, controlled trial comparing vapocoolant spray versus placebo spray in adults undergoing intravenous cannulation
  5. Clinical pain research
  6. The Functional Barometer — An analysis of a self-assessment questionnaire with ICF-coding regarding functional/activity limitations and quality of life due to pain — Differences in age gender and origin of pain
  7. Clinical pain research
  8. Clinical outcome following anterior arthrodesis in patients with presumed sacroiliac joint pain
  9. Observational study
  10. Chronic disruptive pain in emerging adults with and without chronic health conditions and the moderating role of psychiatric disorders: Evidence from a population-based cross-sectional survey in Canada
  11. Educational case report
  12. Management of patients with pain and severe side effects while on intrathecal morphine therapy: A case study
  13. Clinical pain research
  14. Behavioral inhibition, maladaptive pain cognitions, and function in patients with chronic pain
  15. Observational study
  16. Comparison of patients diagnosed with “complex pain” and “somatoform pain”
  17. Original experimental
  18. Patient perspectives on wait times and the impact on their life: A waiting room survey in a chronic pain clinic
  19. Topical review
  20. New evidence for a pain personality? A critical review of the last 120 years of pain and personality
  21. Clinical pain research
  22. A multi-facet pain survey of psychosocial complaints among patients with long-standing non-malignant pain
  23. Clinical pain research
  24. Pain patients’ experiences of validation and invalidation from physicians before and after multimodal pain rehabilitation: Associations with pain, negative affectivity, and treatment outcome
  25. Observational study
  26. Long-term treatment in chronic noncancer pain: Results of an observational study comparing opioid and nonopioid therapy
  27. Clinical pain research
  28. COMBAT study – Computer based assessment and treatment – A clinical trial evaluating impact of a computerized clinical decision support tool on pain in cancer patients
  29. Original experimental
  30. Quantitative sensory tests fairly reflect immediate effects of oxycodone in chronic low-back pain
  31. Editorial comment
  32. Spatial summation of pain and its meaning to patients
  33. Original experimental
  34. Effects of validating communication on recall during a pain-task in healthy participants
  35. Original experimental
  36. Comparison of spatial summation properties at different body sites
  37. Editorial comment
  38. Behavioural inhibition in the context of pain: Measurement and conceptual issues
  39. Clinical pain research
  40. A randomized study to evaluate the analgesic efficacy of a single dose of the TRPV1 antagonist mavatrep in patients with osteoarthritis
  41. Editorial comment
  42. Quantitative sensory tests (QST) are promising tests for clinical relevance of anti–nociceptive effects of new analgesic treatments
  43. Educational case report
  44. Pregabalin as adjunct in a multimodal pain therapy after traumatic foot amputation — A case report of a 4-year-old girl
  45. Editorial comment
  46. Severe side effects from intrathecal morphine for chronic pain after repeated failed spinal operations
  47. Editorial comment
  48. Opioids in chronic pain – Primum non nocere
  49. Editorial comment
  50. Finally a promising analgesic signal in a long-awaited new class of drugs: TRPV1 antagonist mavatrep in patients with osteoarthritis (OA)
  51. Observational study
  52. The relationship between chronic musculoskeletal pain, anxiety and mindfulness: Adjustments to the Fear-Avoidance Model of Chronic Pain
  53. Clinical pain research
  54. Opioid tapering in patients with prescription opioid use disorder: A retrospective study
  55. Editorial comment
  56. Sleep, widespread pain and restless legs — What is the connection?
  57. Editorial comment
  58. Broadening the fear-avoidance model of chronic pain?
  59. Observational study
  60. Identifying characteristics of the most severely impaired chronic pain patients treated at a specialized inpatient pain clinic
  61. Editorial comment
  62. The burden of central anticholinergic drugs increases pain and cognitive dysfunction. More knowledge about drug-interactions needed
  63. Editorial comment
  64. A case-history illustrates importance of knowledge of drug-interactions when pain-patients are prescribed non-pain drugs for co-morbidities
  65. Editorial comment
  66. Why can multimodal, multidisciplinary pain clinics not help all chronic pain patients?
  67. Topical review
  68. Individual variability in clinical effect and tolerability of opioid analgesics – Importance of drug interactions and pharmacogenetics
  69. Editorial comment
  70. A new treatable chronic pain diagnosis? Flank pain caused by entrapment of posterior cutaneous branch of intercostal nerves, lateral ACNES coined LACNES
  71. Clinical pain research
  72. PhKv a toxin isolated from the spider venom induces antinociception by inhibition of cholinesterase activating cholinergic system
  73. Clinical pain research
  74. Lateral Cutaneous Nerve Entrapment Syndrome (LACNES): A previously unrecognized cause of intractable flank pain
  75. Editorial comment
  76. Towards a structured examination of contextual flexibility in persistent pain
  77. Clinical pain research
  78. Context sensitive regulation of pain and emotion: Development and initial validation of a scale for context insensitive avoidance
  79. Editorial comment
  80. Is the search for a “pain personality” of added value to the Fear-Avoidance-Model (FAM) of chronic pain?
  81. Editorial comment
  82. Importance for patients of feeling accepted and understood by physicians before and after multimodal pain rehabilitation
  83. Editorial comment
  84. A glimpse into a neglected population – Emerging adults
  85. Observational study
  86. Assessment and treatment at a pain clinic: A one-year follow-up of patients with chronic pain
  87. Clinical pain research
  88. Randomized, double-blind, placebo-controlled, dose-escalation study: Investigation of the safety, pharmacokinetics, and antihyperalgesic activity of L-4-chlorokynurenine in healthy volunteers
  89. Clinical pain research
  90. Prevalence and characteristics of chronic pain: Experience of Niger
  91. Observational study
  92. The use of rapid onset fentanyl in children and young people for breakthrough cancer pain
  93. Original experimental
  94. Acid-induced experimental muscle pain and hyperalgesia with single and repeated infusion in human forearm
  95. Original experimental
  96. Swearing as a response to pain: A cross-cultural comparison of British and Japanese participants
  97. Clinical pain research
  98. The cognitive impact of chronic low back pain: Positive effect of multidisciplinary pain therapy
  99. Clinical pain research
  100. Central sensitization associated with low fetal hemoglobin levels in adults with sickle cell anemia
  101. Topical review
  102. Targeting cytokines for treatment of neuropathic pain
  103. Original experimental
  104. What constitutes back pain flare? A cross sectional survey of individuals with low back pain
  105. Original experimental
  106. Coping with pain in intimate situations: Applying the avoidance-endurance model to women with vulvovaginal pain
  107. Clinical pain research
  108. Chronic low back pain and the transdiagnostic process: How do cognitive and emotional dysregulations contribute to the intensity of risk factors and pain?
  109. Original experimental
  110. The impact of the Standard American Diet in rats: Effects on behavior, physiology and recovery from inflammatory injury
  111. Educational case report
  112. Erector spinae plane (ESP) block in the management of post thoracotomy pain syndrome: A case series
  113. Original experimental
  114. Hyperbaric oxygenation alleviates chronic constriction injury (CCI)-induced neuropathic pain and inhibits GABAergic neuron apoptosis in the spinal cord
  115. Observational study
  116. Predictors of chronic neuropathic pain after scoliosis surgery in children
  117. Clinical pain research
  118. Hospitalization due to acute exacerbation of chronic pain: An intervention study in a university hospital
  119. Clinical pain research
  120. A novel miniature, wireless neurostimulator in the management of chronic craniofacial pain: Preliminary results from a prospective pilot study
  121. Clinical pain research
  122. Implicit evaluations and physiological threat responses in people with persistent low back pain and fear of bending
  123. Original experimental
  124. Unpredictable pain timings lead to greater pain when people are highly intolerant of uncertainty
  125. Original experimental
  126. Initial validation of the exercise chronic pain acceptance questionnaire
  127. Clinical pain research
  128. Exploring patient experiences of a pain management centre: A qualitative study
  129. Clinical pain research
  130. Narratives of life with long-term low back pain: A follow up interview study
  131. Observational study
  132. Pain catastrophizing, perceived injustice, and pain intensity impair life satisfaction through differential patterns of physical and psychological disruption
  133. Clinical pain research
  134. Chronic pain disrupts ability to work by interfering with social function: A cross-sectional study
  135. Original experimental
  136. Evaluation of external vibratory stimulation as a treatment for chronic scrotal pain in adult men: A single center open label pilot study
  137. Observational study
  138. Impact of analgesics on executive function and memory in the Alzheimer’s Disease Neuroimaging Initiative Database
  139. Clinical pain research
  140. Visualization of painful inflammation in patients with pain after traumatic ankle sprain using [11C]-D-deprenyl PET/CT
  141. Original experimental
  142. Developing a model for measuring fear of pain in Norwegian samples: The Fear of Pain Questionnaire Norway
  143. Topical review
  144. Psychoneuroimmunological approach to gastrointestinal related pain
  145. Letter to the Editor
  146. Do we need an updated definition of pain?
  147. Narrative review
  148. Is acetaminophen safe in pregnancy?
  149. Book Review
  150. Physical Diagnosis of Pain
  151. Book Review
  152. Advances in Anesthesia
  153. Book Review
  154. Atlas of Pain Management Injection Techniques
  155. Book Review
  156. Sedation: A Guide to Patient Management
  157. Book Review
  158. Basics of Anesthesia
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