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Dysfunctional Pain Modulation in Torture Survivors: The Mediating Effect of PTSD
Abstract
Participants:
were 59 torture survivors and 44 age-matched healthy controls (HC). Chronic pain was characterized. Pain threshold, pain tolerance, conditioned pain modulation (CPM) and temporal summation of pain (TSP) were measured. Three PTSD trajectories were identified among torture survivors; chronic, delayed and resilient. Lack of CPM and more intense chronic pain was found among the chronic and delayed groups compared to resilient and HC. TSP was strongest among the chronic group. PTSD trajectories mediated the relationship between torture and CPM. It appears that the duration and severity of posttraumatic distress, rather than the exposure to trauma, are crucial factors that mediate the association between trauma and chronic pain. Since PTSD and its resultant distress are measurable, their evaluation seems particularly important in the management of pain among trauma survivors. The results may be generalized to other instances where chronic pain persists after traumatic events.
Perspectives:
This article presents the mediation effect of PTSD trajectory on pain modulation among trauma survivors suggesting that it is the duration and severity of PTSD/distress, rather than the exposure to trauma per se, that influence the perception and modulation of pain.
... Seven of these 21 studies were conducted in the United States, 31,34,37,42,43,50,51 2 studies were conducted in Australia, 11,49 3 studies were performed in Israel, 5-7 and 9 studies were performed in Europe. 9,13,15,20,24,28,29,45,53 Veterans/victims of war/torture were assessed in 9 studies 5,6,13,29,31,42,43,50 ; PTSDs that were closely linked to traffic accidents were assessed in 4 studies, 11,20,47,48,53 and 4 studies assessed samples with "mixed" trauma types. In 4 studies, the type of trauma was not sufficiently described (see also Table S1 of the supplemental material, available at http://links.lww.com/PR9/A78). ...
... Compared to controls, 2 studies showed lower pain tolerances in individuals with PTSD, 9,53 3 studies showed higher pain threshold in PTSD, 15,37,42 and 2 studies found no significant differences between the 2 group. 6,24 The funnel plot was symmetrical with no evidence of relevant small study bias (Egger test: P 5 0.708). ...
... No meta-analysis was possible due to the small number of included studies. Vaegter et al. 53 observed no differences in CPM comparing patients with accident-related back pain with PTSD to those without PTSD (Hedges g 5 20.13 6 0.04), whereas Defrin et al. 6 observed reduced CPM in individuals with chronic combat-/torture-related PTSD and delayed-onset PTSD compared (Hedges g 5 21.19 6 0.18) to 2 PTSD-free groups (resilient and healthy controls). ...
Posttraumatic stress disorder (PTSD) is a known risk factor for the development of chronic pain conditions, and almost 1 in 5 individuals with chronic pain fulfills the criteria for PTSD. However, the relationship between PTSD and pain is poorly understood and studies on pain perception in patients with PTSD show inconsistent results suggesting that different sensory profiles exist among individuals with PTSD. Here, we (1) systematically summarize the current literature on experimentally evoked pain perception in patients with PTSD compared to subjects without PTSD, and (2) assess whether the nature of the traumatic event is associated with different patterns in pain perception. The main outcome measures were pain threshold, pain tolerance, and pain intensity ratings as well as measures of temporal summation of pain and conditioned pain modulation. A systematic search of MEDLINE, EMBASE, Web of Science, PsycINFO, and CINAHL identified 21 studies for the meta-analysis, including 422 individuals with PTSD and 496 PTSD-free controls. No main effect of PTSD on any outcome measure was found. However, stratification according to the nature of trauma revealed significant differences of small to medium effect sizes. Combat-related PTSD was associated with increased pain thresholds, whereas accident-related PTSD was associated with decreased pain thresholds. No clear relationship between PTSD and experimentally evoked pain perception exists. The type of trauma may affect pain thresholds differently indicating the presence of different subgroups with qualitative differences in pain processing.
... Sequelae after torture are manifold, and they represent a complex challenge for the healthcare system. Torture exposure is significantly associated with post-traumatic stress disorder (PTSD) [2,3,7,[13][14][15][16][17], and torture is considered one of the most traumatizing exposures, with a particularly high risk of developing mental health symptoms and, later, PTSD [6,[16][17][18][19][20]. Such mental health problems as memory disturbances, difficulty in concentrating, lack of energy, sexual dysfunction, emotional irritability, loss of trust, insomnia, nightmares, phobias [12,21], depression [1], anxiety, and psychosis [18] are common among torture survivors. ...
... Such mental health problems as memory disturbances, difficulty in concentrating, lack of energy, sexual dysfunction, emotional irritability, loss of trust, insomnia, nightmares, phobias [12,21], depression [1], anxiety, and psychosis [18] are common among torture survivors. The most common somatic consequences of torture are neuropsychological pathology, broken bones, joint and muscle pain, headaches, dizziness, burns, and hearing loss [15,19,20,22]. ...
Little research has focused on torture survivors’ re-traumatization experiences in health and hospital units that treat somatic diseases, though any medical procedure can re-traumatize survivors. This study’s purpose was to summarize qualitative research evidence on torture survivors’ somatic healthcare experiences and to identify “triggers” or “reminders” that can lead to re-traumatization. The study’s search strategies identified 6,326 citations and eight studies, comprising data from 290 participants, exploring encounters with healthcare providers from torture survivors’ perspectives, which were included in the present research. Dallam’s Healthcare Retraumatization Model was used as a framework for data extraction and analysis. Five main themes were elicited from the findings: (1) invisibility , silence , and mistrust ; (2) healthcare providers’ attitudes and a lack of perceived quality in healthcare ; (3) disempowerment ; (4) avoidance ; and (5) satisfaction and gratitude . An analysis of the study’s findings revealed that torture survivors do not receive adequate healthcare and may experience challenges during treatment that can result in re-traumatization. The findings of this literature review provide a basis for understanding the difficulties that survivors experience in receiving somatic healthcare, as well as an explanation of the re-traumatization process.
... *p < .05. compared to those without pain (Ofek & Defrin, 2007). Potentially contributing to these findings is the fact that the TBI participants in our study were civilians not affected by combat-related posttraumatic stress disorder, a potential contributor to exaggerated pain responses after TBI (Defrin et al., 2017;Defrin et al., 2015). ...
Background
Chronic pain after moderate-to-severe traumatic brain injury (TBI) is associated with notable sensory alterations. Although the incidence of TBI is rapidly growing in older populations, elderly individuals have been largely excluded from sensory testing studies, thus limiting evidence regarding the influence of age on pain-related sensory alterations after TBI. This study aimed to investigate the effect of age on the sensory profiles of patients with and without chronic pain after moderate-to-severe TBI.
Methods
Thermal and mechanical quantitative sensory testing were performed on the painful and contralateral body regions in TBI participants with pain (TBI-P) and on both forearms in TBI participants without pain (TBI-NP). Descriptive information about chronic pain and psychological comorbidities was assessed using validated questionnaires.
Results
Participants included 37 young (18–59 years, 57% with chronic pain) and 22 elderly (≥60 years, 46% with chronic pain) survivors of moderate-to-severe TBI. TBI-P participants exhibited significant alterations in heat and pressure pain sensitivity compared to TBI-NP participants, with more pronounced decreases in heat detection in the elderly group and increased warmth sensitivity in the young group. Alterations were not always associated with chronic pain, as cold hypoesthesia was found in elderly TBI-NP participants. In both age groups, chronic pain was associated with higher levels of depressive mood.
Conclusions
Results suggest that young and elderly TBI survivors have both common and unique sensory properties, highlighting the need to pursue sensory testing studies in older patient groups. Depression might also be an important target for pain management after TBI.
... Pain can be defined as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage" (Loeser and Treede, 2008, p. 475), and is a particularly pertinent issue in biomedical science (Hawkins, 2002;Stokes et al., 2009). Research in both humans and animals suggests that identification of pain states can be challenging as individuals vary in pain sensitivity, tolerance or expression due to life history, social connectedness, sex, health, genotype, and temperament (Mogil and Kest, 1999;Mogil et al., 2000;DeWall and Baumeister, 2006;Defrin et al., 2017;Lush and Ijichi, 2018). The alleviation of pain should be based on the needs of the individual in terms of frequency or dosage (Roughan and Flecknell, 2002;Pham et al., 2010), and Refinement protocols should consider the potential for minimizing undesirable side effects from analgesia administration (Fleming and Coombs, 1992;Cooper et al., 2009;Schaap et al., 2012). ...
Being able to assess pain in nonhuman primates undergoing biomedical procedures is important for preventing and alleviating pain, and for developing better guidelines to minimise the impacts of research on welfare in line with the 3Rs principle of Refinement. Nonhuman primates are routinely used biomedical models however it remains challenging to recognise negative states, including pain, in these animals. This study aimed to identify behavioural and facial changes that could be used as pain or general wellness indicators in the rhesus macaque (Macaca mulatta). Thirty-six macaques scheduled for planned neuroscience procedures were opportunistically monitored at four times: Pre-Operative (PreOp), Post-Operative (PostOp) once the effects of anaesthesia had dissipated, Pre-Analgesia (PreAn) on the subsequent morning prior to repeating routine analgesic treatment, and Post-Analgesia (PostAn) following administration of analgesia. Pain states were expected to be absent in PreOp, moderate in PreAn, and mild or absent in PostOp and PostAn when analgesia had been administered. Three potential pain indicators were identified: lip tightening and chewing, which were most likely to occur in PreAn, and running which was least likely in PreAn. Arboreal behaviour indicated general wellness, while half-closed eyes, leaning of the head or body shaking indicated the opposite. Despite considerable individual variation, behaviour and facial expressions could offer important indicators of pain and wellness and should be routinely quantified, and appropriate interventions applied to prevent or alleviate pain, and promote positive welfare.
... In a longitudinal study spanning 17 years in a three-wave design to assess PTSD after torture experiences, pain thresholds of torture survivors with chronic PTSD, delayed PTSD, resilient survivors, as well as HC were studied at the last assessment within the study. Pain thresholds were similar across all four groups indicating that neither the trauma exposure per se (i.e., torture and captivity) nor PTSD were associated with changes in pain sensitivity (Defrin, Lahav, & Solomon, 2017). To sum up, the existing literature depicts a rather inconsistent picture with regard to alterations in pain sensitivity, either subjective ratings or pain thresholds, at baseline following PTE and PTSD. ...
Experiences of childhood abuse may have detrimental effects on the psychopathological and psychophysiological level. Evidence from previous studies mainly supports the notion that CA-exposed individuals show higher psychopathological impairment, such as intrusive experiences, dissociation, impaired general functioning, as well as reduced satisfaction with QoL and sexuality, as compared to individuals who have not been exposed to CA. On a psychophysiological level, this impairment is reflected by elevated HR and reduced HRV levels. Additionally, altered pain sensitivity has been associated with a history of CA. As a major limitation, the majority of these studies did not assess or control for effects of mental disorders (i.e., PTSD), preventing from disentangling effects of trauma and a PTSD diagnosis. Another branch of research has explicitly assessed these variables in individuals with PTSD related to CA and other kind of PTE and has found comparable results in the respective variables. However, up to this point, there is a research gap of studies on CA-exposed individuals both with and without PTSD that may disentangle the effects of the mere exposure to CA per se against the effects of a consequential PTSD diagnosis. The aim of this dissertation was to examine a broad range of relevant psychopathological and psychophysiological sequelae of childhood abuse in women without mental disorders in order to disentangle the effects of trauma and psychopathology. For this purpose, two studies were conducted in order to focus on relevant psychopathological and psychophysiological aspects that are known to be impaired after experiencing CA and in patients with PTSD related to CA. These relevant aspects encompassed a broad range of general and PTSD-specific psychopathology, general functioning, quality of life, and satisfaction with sexuality. Additionally, stress responsiveness was examined at the subjective and psychophysiological level in response to experimentally induced stress. Furthermore, pain sensitivity at baseline as well as in response to stress were examined. These features were examined in HTEW as compared to HC women without a history of CA and female patients with PTSD related to experiences of CA. In study I, HTEW showed a high level of functioning and a very low level of pathological impairment that was comparable to the level of healthy controls. The results of study I in this dissertation suggest that PTE exposure per se does not necessarily have to go along with the development of psychopathology or impaired quality of life, sexuality, self-esteem, or guilt cognitions. Results of the present study rather suggest an association of PTSD and impairment in the reported variables. In the second study, the most distinct and clinically meaningful effects between HTEW and PTSD-patients were observed concerning subjective stress parameters. With regard to subjective ratings of stress and dissociation, HTEW were clearly different from PTSD-patients while resembling the group of HC. With respect to the psychophysiological parameters (HR and HRV) and pain sensitivity, the picture was less clear: Although HTEW differed significantly from PTSD-patients with respect to HR and HRV, differences were not as pronounced as for the subjective ratings. With respect to pain sensitivity in response to experimentally induced stress, comparisons of HTEW and PTSD-patients only approached significance. In comparison to HC, HTEW differed significantly for HR, HRV, and pain sensitivity. On a descriptive level, HR, HRV and pain sensitivity levels of HTEW were located in between levels of HC and of PTSD-patients. Results of the second study of this dissertation reveal that differences between HTEW and PTSD-patients in baseline stress levels as well as stress responses were most distinct in subjective as compared to psychophysiological readouts. This may imply that subjective stress rating and dissociation may be seen as diagnostic correlates of PTSD rather than being related to experiences of CA per se. Results of the objective stress indicators draw a less clear picture: Although HTEW differed significantly from PTSD-patients and HC with respect to HR and HRV, differences between HTEW and PTSD-patients were not as pronounced as for the subjective indicators of stress. Taken together, based on recent advances in this field as well as results of our own work, it is proposed that psychopathology in form of a PTSD diagnosis seems to contribute to more general psychopathology (i.e., intrusions and dissociation), impaired general functioning, reduced QoL and satisfaction with sexuality, impaired baseline stress levels as well as stress responsiveness on a subjective as well as psychophysiological level. However, results of study II also suggest that one cannot exclude an additional role of CA on psychophysiological stress responses as well as pain sensitivity as the data also indicates that a small proportion of altered stress response may relate to experiences of CA per se. The contribution of this dissertation is an increased knowledge on the sequelae of CA apart from developing PTSD. Improved knowledge on the sequelae of CA may help identifying novel diagnostic markers to detect individuals who are at risk of developing PTSD. An early detection of vulnerability to PTSD in turn would help prevent developing a full-blown PTSD, as preventive programs could be called into action at an earlier stage. Furthermore, the recognition of these mechanisms and sequelae can help improve treatment planning in terms of potential accompanying symptoms that are not entailed as diagnostic criteria of PTSD (i.e., reduced self-esteem, reduced satisfaction with QoL and sexuality). Furthermore, results of this dissertation suggest that good self-esteem, absence of guilt cognitions, as well as the process of disclosure seem to be important in withstanding adversities unscathed. With potentially important implications for treatment, these findings highlight the importance of routinely inquiring about CA as well as educating and training support-providers and society about sexual and physical assault. Training programs should encompass how to respond to disclosure of CA in more supportive ways. Furthermore, the implementation of prevention programs focused on developing and supporting the adolescent’s sense of being a good and worthy person should be encouraged.
... However, a review of the literature on the relationship between pain and PTSD found inconsistencies and proposed that it is likely to be a complex interplay in which pain perception may be affected by the duration and severity of PTSD and other influences on individual susceptibility (Moeller-Bertram 2012). Another study compared war veterans who had been tortured with a control group who had not (Defrin 2017). Findings from two psychophysiological tests (i.e. ...
More than 68 million people worldwide have been forcibly displaced and one-third of these are refugees. This article offers an overview of the current literature and reviews the epidemiology and evidence-based psychological and pharmacological management of post-traumatic stress disorder (PTSD), sleep disturbance and pain in refugees and asylum seekers. It also considers the relationship between sleep disturbance and PTSD and explores concepts of pain in relation to physical and psychological trauma and distress. During diagnosis, clinicians must be aware of ethnic variation in the somatic expression of distress. Treatments for PTSD, pain and sleep disturbance among refugees and asylum seekers are essentially the same as those used in the general population, but treatment strategies must allow for cultural and contextual factors, including language barriers, loss of freedom and threat of repatriation.
LEARNING OBJECTIVES
After reading this article you will be able to: • recognise the challenges faced by the large number of refugees worldwide
• understand the relationship between PTSD, sleep disturbance and pain in refugees
• broadly understand the evidence for psychological and pharmacological therapy for treating PTSD, sleep disturbance and pain in refugees.
DECLARATION OF INTEREST
None.
... ain is defined according to the International Association for the Study of Pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage (1)(2)(3)(4). Fibromyalgia is an idiopathic condition of widespread musculoskeletal pain. The first classification criteria for diagnosing fibromyalgia were published in 1990 by the American College of Rheumatology (ACR) (5). ...
Introduction: The Fibromyalgia Rapid Screening Tool (FiRST) is a brief, simple, and straight forward self-administered questionnaire that was developed by Perrot et al. for the detection of fibromyalgia syndrome in patients with diffuse chronic pain. Aim: The aim of our study was to develop and validate the Egyptian version of FiRST. Methods: The study was set up as a prospective observational study. The original French version of FiRST was adapted into Egyptian using forward and backward translation. Patients with chronic diffuse pain with a clinical diagnosis of fibromyalgia and osteoarthritis based on the criteria of the American College of Rheumatology were invited to participate to the study. Results: 140 patients who met our inclusion criteria, 80 were diagnosed with fibromyalgia and 60 with osteoarthritis. The 2 groups were matched gender and pain characteristics (duration, intensity). Cronbach’s alpha coefficient was 0.83. Receiver operating characteristic analysis showed an area under the curve of 89% (95% confidence interval = 83 to 95%; SE: 0.032, P < 0.001). At a cutoff score of ≥ 5, FiRST showed a sensitivity of 86%, a specificity of 83%, a positive predictive value of 78%, and a negative predictive value of 89%. The intra class coefficient for the test–retest reliability was 0.96. Conclusion: The Egyptian version of FiRST is a valid screening tool for fibromyalgia in daily practice.
... This finding is theoretically important because congruent with a PTSD diagnosis is a related propensity to experience chronic pain as suggested in previous theoretical models of the PTSD-pain relationship (Asmundson et al., 2002). Another interpretation of the importance of PTSD and its relationship to pain was suggested in a recent study of torture victims (Defrin, Lahav, & Solomon, 2016) where it is suggested that PTSD moderated the relationship between trauma exposure and pain by altering pain modulation. ...
Background: Trauma exposure and post-traumatic stress disorder (PTSD) are risk factors for chronic pain.
Objective: This study investigated how exposure to intentional and non-intentional traumatic events and PTSD are related to pain severity and outcome of treatment in chronic pain patients.
Methods: We assessed exposure to potentially traumatizing events, psychiatric diagnosis with structured clinical interview, and pain severity in 63 patients at a secondary multidisciplinary pain clinic at the beginning of treatment, and assessed level of pain at follow up. Exposure to potentially traumatizing events and PTSD were regressed on pain severity at the initial session and at follow up in a set of multiple regression analysis.
Results: The participants reported exposure to an average of four potentially traumatizing events, and 32% had PTSD. Exposure to intentional traumatic events and PTSD were significantly associated with more severe pain, and PTSD significantly moderated the relationship between trauma exposure and pain (all p < .05). The treatment programme reduced pain moderately, an effect that was unrelated to trauma exposure and PTSD.
Conclusions: Trauma exposure is related to chronic pain in the same pattern as to mental disorders, with intentional trauma being most strongly related to pain severity. PTSD moderated the relationship between trauma exposure and pain. While pain patients with PTSD initially report more pain, they responded equally to specialist pain treatment as persons without PTSD.
Urologic chronic pelvic pain syndrome (UCPPS) is a complex, debilitating condition in which patients often report nonpelvic pain in addition to localized pelvic pain. Understanding differential predictors of pelvic pain only vs widespread pain may provide novel pathways for intervention. This study leveraged baseline data from the Multidisciplinary Approach to the Study of Chronic Pelvic Pain (MAPP) Research Network's Symptom Pattern Study to investigate the impact of childhood sexual and nonsexual violent trauma on pelvic and nonpelvic pain sensitivity among adult patients with UCPPS, as well as potential mediators of this association. Study participants who met inclusion criteria for UCPPS completed questionnaires assessing childhood and recent trauma, affective distress, cognitive dysfunction, and generalized sensory sensitivity. Experimental pain sensitivity was also evaluated using standardized pressure pain applied to the pubic region and the arm. Bivariate analyses showed that childhood violent trauma was associated with more nonviolent childhood trauma, more recent trauma, poorer adult functioning, and greater pain sensitivity at the pubic region, but not pain sensitivity at the arm. Path analysis suggested that childhood violent trauma was indirectly associated with pain sensitivity at both sites and that this indirect association was primarily mediated by generalized sensory sensitivity. More experiences of recent trauma also contributed to these indirect effects. The findings suggest that, among participants with UCPPS, childhood violent trauma may be associated with heightened pain sensitivity to the extent that trauma history is associated with a subsequent increase in generalized sensory sensitivity.
Equine‐assisted therapy (EAT) is an increasingly popular form of treatment for people suffering from post‐traumatic stress disorder (PTSD) who, for one reason or another, find psychotherapy and other traditional treatment approaches unsuitable or unhelpful. However, the concomitant growth of research in the field is yet to engage with key factors relating to EAT; specifically, there are few studies considering the phenomenological perspective of patients, and the embodied knowledge deriving from the lived experience of PTSD patients who participated in EAT‐based intervention programmes. Based on a qualitative‐phenomenological study, interviews were conducted with 12 PTSD patients who had completed an EAT‐based intervention programme. From these, three main themes characterising the meanings they gave to participation in an EAT‐based treatment programme were identified: the ability to relax (self‐regulation); establishing a relationship (bonding) and transformation and hope for the future. The findings of this study point to a process whereby participation in an EAT‐based treatment programme facilitates the ability to cope with PTSD symptoms in a way that bridges the patient's emotional, social and spiritual‐existential dimensions. The findings suggest that EAT can contribute to the healing process of veterans suffering from PTSD.
Several reports indicate either increased or decreased pain sensitivity associated with psychiatric disorders. Chronic pain is highly prevalent in many of these conditions. We reviewed the literature regarding experimental pain sensitivity in patients with major depression, bipolar disorder, posttraumatic stress disorder (PTSD), generalized anxiety disorder, panic disorder, obsessive-compulsive disorder and schizophrenia. Electronic searches were performed to identify studies comparing experimental pain in patients with these conditions and controls. Across 31 depression studies, reduced pain threshold was noted except for ischemic stimuli, where increased pain tolerance and elevated sensitivity to ischemic pain was observed. A more pervasive pattern of low pain sensitivity was found across 20 schizophrenia studies. The majority of PTSD studies (n = 20) showed no significant differences compared with controls. The limited number of bipolar disorder (n = 4) and anxiety (n = 9) studies precluded identification of clear trends. Wide data variability was observed. Awareness of psychiatric patients’ pain perception abnormalities is needed for active screening and addressing physical comorbidities, in order to enhance quality of life, life expectancy and mental health.
Inflicting pain as a mechanism for the development of power-relationships is not new. When examined using the aggressor-witness-victim model, relationships based on the control of the aggressor can be examined with regard to the ability to either inflict pain or to withhold pain. The aggressor has the power in violent interaction to either cause pain or to not cause pain. This ability creates a dependency between these groups as well as the witnesses who are present for the interaction. This dependency is a public performance in which it is made clear that the aggressor has control over the physical body of the victim and the witnesses. This relationship is explored both prehistorically through the lens of the Sacred Ridge site (dating to 800 AD in southwestern Colorado) and modern examples. In many ways, witnessing the pain of another is more psychologically damaging that experiencing pain firsthand, and may lead to more easily allowing for the social control of one group over another.
Trauma survivors may suffer from posttraumatic stress disorder (PTSD), elevated posttraumatic guilt (PG), and alterations in the pain system. However, the association between PG and alterations in pain perception and modulation among trauma survivors has not been
established, nor has the possible underlying role of PG. This longitudinal study investigated:
1) the unique contribution of PG in predicting pain perception and modulation, while controlling for PTSD symptoms; and 2) the mediating role of PG in explaining pain perception and modulation among torture survivors, above and beyond PTSD symptoms.
Participants were 59 torture survivors and 44 age-matched controls. PG and PTSD symptoms were assessed in 2003 (T1). Heat-pain threshold, heat-pain tolerance, temporal summation of pain (TSP) and conditioned pain modulation (CPM) were measured five years later (T2).
Torture survivors had elevated PG and PTSD symptoms, enhanced TSP, and reduced CPM, compared to controls. While PTSD predicted reduced pain tolerance and CPM, PG predicted increased pain tolerance. Moreover, PG mediated the associations between torture and (increased) pain threshold, pain tolerance, and TSP. It appears that PTSD and PG induce opposite effects on the pain modulation capacity of torture survivors, a dichotomy that may explain paradoxical pain responses among trauma survivors, as discussed.
Perspective: This longitudinal study sheds light on the possible mechanisms underlying variations in pain perception and modulation among trauma survivors. PTSD and posttraumatic guilt each mediated opposing pain modulation profiles, suggesting that individual responses to trauma, rather than the trauma itself, influence pain responses.
Political persecution, torture, war and civil war are a growing problem, contributing also significantly to the present international refugee crises. The severe long-term impact on social systems, physical and especially psychological health, which can even become transgenerational, has been well documented. Violence in this context can be seen as the probably most significant global risk factor in mental health. Addressing prevention, support, treatment and long-term rehabilitation requires an interdisciplinary effort and close collaboration between health-care, legal and other experts, as well as of international organisations and UN bodies. The increasing importance of transcultural factors is of special relevance in the development of programmes in war areas and for displaced populations. Protection for vulnerable groups and human rights standards must be supported in different settings including asylum procedures.
By unconscious or covert processing of pain we refer to nascent interactions that affect the eventual deliverance of pain awareness. Thus, internal processes (viz., repeated nociceptive events, inflammatory kindling, reorganization of brain networks, genetic) or external processes (viz., environment, socioeconomic levels, modulation of epigenetic status) contribute to enhancing or inhibiting the presentation of pain awareness. Here we put forward the notion that for many patients, ongoing sub-conscious changes in brain function are significant players in the eventual manifestation of chronic pain. In this review, we provide clinical examples of nascent or what we term pre-pain processes and the neurobiological mechanisms of how these changes may contribute to pain, but also potential opportunities to define the process for early therapeutic interventions.
The effect of acute stress on pain threshold and intolerance threshold are reported as producing either hypoalgesia or hyperalgesia. Yet, the contribution of individual stress reactivity in this respect has not been established. The aim was to test 2 pain modulation paradigms under acute stress manipulation, to our knowledge, for the first time, to study whether stress differentially affects pain modulation, and whether the effect is related to individual stress response. Participants were 31 healthy subjects. Conditioned pain modulation (CPM) and pain adaptation were measured before and after inducing an acute stress response using the Montreal Imaging Stress Task. Subjects' stress response was evaluated according to salivary cortisol, autonomic function, and perceived stress and anxiety. The Montreal Imaging Stress Task induced a validated stress response. On a group level, stress induced reduction in CPM magnitude and increase in pain adaptation compared with baseline. These responses correlated with stress reactivity. When the group was subdivided according to stress reactivity, only high stress responders exhibited reduced CPM whereas only low stress responders exhibited increased pain adaptation. The results suggest that acute stress may induce opposite effects on pain modulation, depending on individual stress reactivity magnitude, with an advantage to low stress responders.
Perspectives
This study evaluated the effect of acute stress on pain modulation. Pain modulation under stress is affected by individual stress responsiveness; decreased CPM occurs in high stress responders whereas increased pain adaptation occurs in low stress responders. Identification of high stress responders may promote better pain management.
Background:
Persistent (chronic) pain is a frequent complaint in survivors of torture, particularly but not exclusively pain in the musculoskeletal system. Torture survivors may have no access to health care; where they do, they may not be recognised when they present, and the care available often falls short of their needs. There is a tendency in state and non-governmental organisations' services to focus on mental health, with poor understanding of persistent pain, while survivors may have many other legal, welfare, and social problems that take precedence over health care.
Objectives:
To assess the efficacy of interventions for treating persistent pain and associated problems in survivors of torture.
Search methods:
We searched for randomised controlled trials (RCTs) published in any language in CENTRAL, MEDLINE, Embase, Web of Science, CINAHL, LILACS, and PsycINFO, from database inception to 1 February 2017. We also searched trials registers and grey literature databases.
Selection criteria:
RCTs of interventions of any type (medical, physical, psychological) compared with any alternative intervention or no intervention, and with a pain outcome. Studies needed to have at least 10 participants in each arm for inclusion.
Data collection and analysis:
We identified 3578 titles in total after deduplication; we selected 24 full papers to assess for eligibility. We requested data from two completed trials without published results.We used standard methodological procedures expected by Cochrane. We assessed risk of bias and extracted data. We calculated standardised mean difference (SMD) and effect sizes with 95% confidence intervals (CI). We assessed the evidence using GRADE and created a 'Summary of findings' table.
Main results:
Three small published studies (88 participants) met the inclusion criteria, but one had been retracted from publication because of ethical problems concerned with confidentiality and financial irregularities. Since these did not affect the data, the study was retained in this review. Despite the search including any intervention, only two types were represented in the eligible studies: two trials used cognitive behavioural therapy (CBT) with biofeedback versus waiting list on unspecified persistent pain (58 participants completed treatment), and one examined the effect of complex manual therapy versus self-treatment on low back pain (30 participants completed treatment). Excluded studies were largely either not RCTs or did not report pain as an outcome.There was no difference for the outcome of pain relief at the end of treatment between CBT and waiting list (two trials, 58 participants; SMD -0.05, 95% CI -1.23 to 1.12) (very low quality evidence); one of these reported a three-month follow-up with no difference between intervention and comparison (28 participants; SMD -0.03, 95% CI -0.28 to 0.23) (very low quality evidence). The manual therapy trial also reported no difference between complex manual therapy and self-treatment (30 participants; SMD -0.48, 95% CI -9.95 to 0.35) (very low quality evidence). Two studies reported dropouts, one with partial information on reasons; none of the studies reported adverse effects.There was no information from any study on the outcomes of use of analgesics or quality of life.Reduction in disability showed no difference at the end of treatment between CBT and waiting list (two trials, 57 participants; SMD -0.39, 95% CI -1.17 to 0.39) (very low quality evidence); one of these reported a three-month follow-up with no difference between intervention and comparison (28 participants; SMD 0, 95% CI -0.74 to 0.74) (very low quality evidence). The manual therapy trial reported superiority of complex manual therapy over self-treatment for reducing disability (30 participants; SMD -1.10, 95% CI - 1.88 to -0.33) (very low quality evidence).Reduction in distress showed no difference at the end of treatment between CBT and waiting list (two trials, 58 participants; SMD 0.07, 95% CI -0.46 to 0.60) (very low quality evidence); one of these reported a three-month follow-up with no difference between intervention and comparison (28 participants; SMD -0.24, 95% CI -0.50 to 0.99) (very low quality evidence). The manual therapy trial reported superiority of complex manual therapy over self-treatment for reducing distress (30 participants; SMD -1.26, 95% CI - 2.06 to -0.47) (very low quality evidence).The risk of bias was considered high given the small number of trials, small size of trials, and the likelihood that each was underpowered for the comparisons it reported. We primarily downgraded the quality of the evidence due to small numbers in trials, lack of intention-to-treat analyses, high unaccounted dropout, lack of detail on study methods, and CIs around effect sizes that included no effect, benefit, and harm.
Authors' conclusions:
There is insufficient evidence to support or refute the use of any intervention for persistent pain in survivors of torture.
Background and aim:
The Fibromyalgia Rapid Screening Tool (FiRST) is a brief, simple and straightforward self-administered questionnaire that was developed by Perrot et al. for the detection of fibromyalgia syndrome in patients with diffuse chronic pain. The aim of our study was to develop and validate the Greek version of FiRST.
Methods:
The study was set up as a prospective observational study. The original French version of FiRST was adapted into Greek using forward and backward translation. Patients with chronic diffuse pain with a clinical diagnosis of fibromyalgia and osteoarthritis based on the criteria of the American College of Rheumatology were invited to participate to the study.
Results:
Of the 101 patients who met our inclusion criteria, 42 were diagnosed with fibromyalgia and 59 with osteoarthritis. The 2 groups did not differ significantly regarding gender and pain characteristics (duration, intensity). Cronbach's alpha coefficient was 0.79. Receiver operating characteristic analysis showed an area under the curve of 89% (95% confidence interval = 83%-95%; SE: 0.032, P < 0.001). At a cutoff score of ≥5, FiRST showed a sensitivity of 86%, a specificity of 83%, a positive predictive value of 78%, and a negative predictive value of 89%. The intraclass coefficient for the test-retest reliability was 0.96.
Conclusion:
The Greek version of FiRST is a valid screening tool for fibromyalgia in daily practice. This article is protected by copyright. All rights reserved.
Despite substantial research on the comorbidity of anxiety disorders including posttraumatic stress disorder (PTSD) and chronic pain, little is known about the mechanisms underlying these conditions that might be potentially similar. Evoked pain sensitivity is one factor that has been associated with several pain conditions which might also have relevance to anxiety disorders and PTSD. The aim of this preliminary study was to examine evoked pain sensitivity in PTSD compared to other anxiety disorders and in control participants.
The study used a cross-sectional case-control design in which participants completed a battery of questionnaires and structured interview and underwent cold pressor testing.
Of 61 total participants, those in the PTSD (n =16) and other anxiety groups (n =12) endorsed significantly higher levels of psychological symptoms and poorer health functioning than control participants (n =33). The linear trend across baseline, threshold, and tolerance pain ratings from the cold pressor task significantly differed between participants with PTSD and the other anxiety and control groups suggesting lower pain sensitivity to a standardized stimulus of pain in individuals with PTSD.
These findings are similar to some of the prior research and suggest that individuals with PTSD may exhibit lower cold pain sensitivity compared to those with other anxiety disorders. There is a need for future research to determine explanatory mechanisms.
Although the prevalence rate of chronic post traumatic headache (CPTHA) after mild traumatic brain injury (TBI) reaches up to 95%, its mechanism is unknown and little is known about the characteristics of the pain system in this condition. Our aim was to investigate the capabilities of two pain modulatory systems among individuals with CPTHA and study their association with CPTHA, here for the first time. Forty-six subjects participated; 16 with TBI and CPTHA, 12 with TBI without CPTHA, and 18 healthy controls. Testing included the measurement of heat-pain (HPT) and pressure-pain (PPT) thresholds in the forehead and forearm, pain adaptation to tonic noxious heat and conditioned pain modulation (CPM). The participants completed a post-traumatic stress disorder (PTSD) questionnaire. The two TBI groups did not differ in the TBI and background characteristics. However, TBI patients with CPTHA had significantly higher HPT and lower PPT in the cranium and higher PTSD symptomatology compared to TBI patients without CPTHA and healthy controls. Adaptation to pain and CPM were diminished in the CPTHA group compared to the two control groups. The intensity of CPTHA correlated negatively with cranial PPT, magnitude of pain adaptation and CPM. CPTHA intensity correlated positively with PTSD symptomatology. CPTHA appears to be are characterized by cranial hyperalgesia and dysfunctional pain modulation capabilities, that are associated with CPTHA magnitude. It is concluded that damage to pain modulatory systems along with chronic cranial sensitization underlies the development of CPTHA. PTSD may reinforce CPTHA and vice versa. Clinical implications are discussed.
Background:
In healthy individuals slow temporal summation of pain or wind-up (WU) can be evoked by repetitive heat-pulses at frequencies of ≥.33 Hz. Previous WU studies have used various stimulus frequencies and intensities to characterize central sensitization of human subjects including fibromyalgia (FM) patients. However, many trials demonstrated considerable WU-variability including zero WU or even wind-down (WD) at stimulus intensities sufficient for activating C-nociceptors. Additionally, few WU-protocols have controlled for contributions of individual pain sensitivity to WU-magnitude, which is critical for WU-comparisons. We hypothesized that integration of 3 different WU-trains into a single WU-response function (WU-RF) would not only control for individuals' pain sensitivity but also better characterize their central pain responding including WU and WD.
Methods:
33 normal controls (NC) and 38 FM patients participated in a study of heat-WU. We systematically varied stimulus intensities of.4 Hz heat-pulse trains applied to the hands. Pain summation was calculated as difference scores of 1st and 5th heat-pulse ratings. WU-difference (WU-Δ) scores related to 3 heat-pulse trains (44°C, 46°C, 48°C) were integrated into WU-response functions whose slopes were used to assess group differences in central pain sensitivity. WU-aftersensations (WU-AS) at 15 s and 30 s were used to predict clinical FM pain intensity.
Results:
WU-Δ scores linearly accelerated with increasing stimulus intensity (p<.001) in both groups of subjects (FM>NC) from WD to WU. Slope of WU-RF, which is representative of central pain sensitivity, was significantly steeper in FM patients than NC (p<.003). WU-AS predicted clinical FM pain intensity (Pearson's r = .4; p<.04).
Conclusions:
Compared to single WU series, WU-RFs integrate individuals' pain sensitivity as well as WU and WD. Slope of WU-RFs was significantly different between FM patients and NC. Therefore WU-RF may be useful for assessing central sensitization of chronic pain patients in research and clinical practice.
Unlabelled:
Many refugees in the developed world are survivors of torture and present with health needs without their traumatic experience being disclosed or identified. Chronic pain is a common problem, as are symptoms of post-traumatic stress disorder (PTSD), anxiety, depression, and other distress. Current circumstances, particularly poverty, uncertainty about asylum, separation from or loss of family and roles, and difficulties settling in the host country, all contribute to current psychological problems and exacerbate existing ones. Psychological treatment studies tend to be focused either on PTSD diagnosis and use protocol-driven treatment, usually in the developed world, or on multiple problems using multimodal treatment including advocacy and welfare interventions, usually in the developing world. Reviews of both of these, and some of the major criticisms, are described. Psychological interventions tend to produce medium-sized changes in targeted measures of distress, when compared with waiting lists or standard treatment, but these may fall well short of enabling recovery, and long-term follow-up is rare. A human rights context, with reference to cultural difference in expressing distress and seeking help, and with reference to the personal meaning of torture, is essential as a basis for formulating treatment initiatives based on the evidence reviewed.
Summary points:
Refugees with a history of torture may have a wide range of psychological and social difficulties which do not easily fit within diagnostic categories.Torture and its sequelae can have multiple meanings and, in the clinical context, it is the interpretation of the torture survivor that matters.There are doubts about applying the concept and measures of post-traumatic stress disorder: symptoms should be assessed separately.Current circumstances can be as important as trauma history in understanding the psychological state of a torture survivor.Cognitive behavioural therapy and narrative exposure therapy seem equally effective in reducing trauma symptoms, and to a lesser extent, depression.
Obesity is a major public health concern and there are increasing calls for policy intervention. As obesity and the related health conditions develop during childhood, schools are being seen as important locations for obesity prevention, including multifaceted interventions incorporating policy elements. The objective of this systematic review was to evaluate the effects of policies related to diet and physical activity in schools, either alone, or as part of an intervention programme on the weight status of children aged 4 to 11 years. A comprehensive and systematic search of medical, education, exercise science, and social science databases identified 21 studies which met the inclusion criteria. There were no date, location or language restrictions. The identified studies evaluated a range of either, or both, diet and physical activity related policies, or intervention programmes including such policies, using a variety of observational and experimental designs. The policies were clustered into those which sought to affect diet, those which sought to affect physical activity and those which sought to affect both diet and physical activity to undertake random effects meta-analysis. Within the diet cluster, studies of the United States of America National School Lunch and School Breakfast Programs were analysed separately; however there was significant heterogeneity in the pooled results. The pooled effects of the physical activity, and other diet related policies on BMI-SDS were non-significant. The multifaceted interventions tended to include policy elements related to both diet and physical activity (combined cluster), and although these interventions were too varied to pool their results, significant reductions in weight-related outcomes were demonstrated. The evidence from this review suggests that, when implemented alone, school diet and physical activity related policies appear insufficient to prevent or treat overweight or obesity in children, however, they do appear to have an effect when developed and implemented as part of a more extensive intervention programme. Additional evidence is required before recommendations regarding the focus of policies can be made and therefore, increased effort should be made to evaluate the effect of policies and policy containing intervention programmes upon weight status.
Falanga torture (beatings on the foot soles) produces local chronic pain and severe walking difficulties. We have previously reported signs of neuropathic pain in the feet of falanga victims. The objective here was to clarify underlying pain mechanisms by quantifying sensory impairments in the feet of torture victims who had experienced both generalized torture and those who had been exposed to falanga in addition. An ethnically matched control group was available.
We employed quantitative sensory testing (QST) by investigators blinded to whether the patients, 32 male torture victims from the Middle East, had (n=15), or had not (n=17) been exposed to falanga. Pain intensity, area and stimulus dependence were used to characterize the pain as were interview data on sensory symptoms. QST included thresholds for touch, cold, warmth, cold-pain, heat-pain, deep pressure pain and wind-up to cutaneous noxious stimuli in the foot soles. Clinical data on anxiety and depression were retrieved.
Almost all falanga victims had moderate or strong pain in their feet and in twice as large an area of their foot soles as other torture victims. One-third of the latter had no pain in their feet and many reported slight pain; in spite of this, there were no differences in foot sole QST data between the tortured groups. A comparison with normal data indicated that both tortured groups had hypoesthesia for all cutaneous sensory fibre groups except those transmitting cold and heat pain, in addition to deep mechano-nociceptive hyperalgesia.
A comparison of the QST data between victims having been exposed to generalized torture and victims who in addition had been exposed to falanga, showed no differences on the group level. The sensory disturbances in relation to our control group are compatible with central sensitization and de-sensitization, pointing to a core role of central mechanisms. A further analysis to create individual sensory profiles from our measurements is in progress.
Reviews studies that relate to the norms, reliability, and validity of the Dissociative Experiences Scale (DES). Appropriate clinical and research use of the scale are discussed together with factor analytic studies and fruitful statistical analysis methods. Research reported for 1989–1992 with the DES is described, and promising new research questions are highlighted. Suggestions are made for translating and using the DES in other cultures. A 2nd version of the DES, which is easier to score, is included as an appendix. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Although war captivity is a potent pathogen for psychiatric illness, little is known about the long-term trajectories of post-traumatic stress disorder (PTSD) among ex-prisoners of wars (ex-POWs). This study aimed to assess the long-term trajectories of PTSD and their predictors following war captivity. One hundred and sixty four Israeli ex-POWs and 185 comparable combatants from the 1973 Yom Kippur War were followed over 35 years, with three follow-ups (1991, 2003, 2008). Ex-POWs reported higher PTSD rates than controls at all three assessments. Four trajectories of PTSD were identified: chronic PTSD, delayed PTSD, recovery and resilience. The majority of POWs reported delayed PTSD, while the majority of controls were classified as resilient. While PTSD rates remained relatively stable over time among controls, a steep increase in rates was observed among POWs between 1991 and 2003, followed by stabilization in rates between 2003 and 2008. Finally, subjective experience of captivity was the variable that best distinguished between the resilience and PTSD groups of ex-POWs, followed by participation in previous wars and negative life events during childhood. War captivity carries long-lasting psychiatric implications, even decades after release. Aging processes, as well as unique stressors that exist in Israel, may account for the elevated PTSD rates found here.
Unlabelled:
Timing of assessment of psychological construct is controversial and results differ based on the model of pain induction. Previous studies have not used an exercise-induced injury model to investigate timing of psychological assessment. Exercise-induced injury models may be appropriate for these investigations because they approximate clinical pain conditions better than other experimental stimuli. In this study we examined the changes of psychological constructs over time and determined whether timing of assessment affected the construct's association with reports of pain intensity and disability. One-hundred twenty-six healthy volunteers completed the Fear of Pain Questionnaire (FPQ-III), Pain Catastrophizing Scale (PCS), and Tampa Scale of Kinesiophobia (TSK) prior to inducing muscle injury to the shoulder. The PCS and TSK were measured again 48 and 96 hours postinjury induction. Pain intensity and disability were collected at 48 and 96 hours and served as dependent variables in separate regression models. Results indicated that the FPQ-III had the strongest prediction of pain intensity from baseline to 96 hours. After baseline the PCS and TSK were stronger predictors of pain intensity and disability, respectively. These data provide support for the use of psychological constructs in predicting outcomes from shoulder pain. However, they deviate from the current theoretical model indicating that fear of pain is a consequence of injury and instead suggests that fear of pain before injury may influence reports of pain intensity.
Perspective:
The current study provides evidence that fear of pain can be assessed prior to injury. Furthermore, it supports that after injury pain catastrophizing and kinesiophobia are independently associated with pain and disability. Overall these data suggest that timing of psychological assessment may be an important consideration in clinical environments.
Cross-sectional designs and self-reports of maltreatment characterize nearly all the literature on childhood abuse or neglect and pain in adulthood, limiting potential for causal inference. The current study describes a prospective follow up of a large cohort of individuals with court-documented early childhood abuse or neglect (n=458) and a demographically matched control sample (n=349) into middle adulthood (mean age 41), nearly 30 years later, comparing the groups for risk of adult pain complaints. We examine whether Post-Traumatic Stress Disorder (PTSD) mediates or moderates risk of pain. Assessed prospectively across multiple pain measures, physically and sexually abused and neglected individuals generally showed a significant (p<.05) but notably small (η(2)=.01) increased risk of pain symptoms in middle adulthood. Although PTSD was associated with both childhood victimization (p<.01) and risk of middle adulthood pain (p<.001), it did not appear to mediate the relationship between victimization and pain. However, across all pain outcomes other than medically unexplained pain, PTSD robustly interacted with documented childhood victimization to predict adult pain risk: Individuals with both childhood abuse/neglect and PTSD were at significantly increased risk (p<.001, η(2) generally=.05-.06) of pain. After accounting for the combined effect of the two factors, neither childhood victimization nor PTSD alone predicted pain risk. Findings support a view that clinical pain assessments should focus on PTSD rather than make broad inquiries into past history of childhood abuse or neglect.
Imaging studies of pain processing in primary psychiatric disorders are just emerging. This study explored the neural correlates of stress-induced analgesia in individuals with posttraumatic stress disorder (PTSD). It combined functional magnetic resonance imaging (fMRI) and the traumatic script-driven imagery symptom provocation paradigm to examine the effects of trauma-related cues on pain perception in individuals with PTSD.
The study included 17 patients with PTSD and 26 healthy, trauma-exposed controls. Participants received warm (nonpainful) or hot (painful) thermal stimuli after listening to a neutral or a traumatic script while they were undergoing an fMRI scan at a 4.0 T field strength.
Between-group analyses revealed that after exposure to the traumatic scripts, the blood oxygen level-dependent (BOLD) signal during pain perception was greater in the PTSD group than the control group in the head of the caudate. In the PTSD group, strong positive correlations resulted between BOLD signal and symptom severity in a number of brain regions previously implicated in stress-induced analgesia, such as the thalamus and the head of the caudate nucleus. Trait dissociation as measured by the Dissociative Experiences Scale correlated negatively with the right amygdala and the left putamen. Limitations: This study included heterogeneous traumatic experiences, a different proportion of military trauma in the PTSD versus the control group and medicated patients with PTSD.
These data indicate that in patients with PTSD trauma recall will lead in a state-dependent manner to greater activation in brain regions implicated in stress-induced analgesia. Correlational analyses lend support to cortical hyperinhibition of the amygdala as a function of dissociation.
Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity, headache, temporomandibular joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and post-surgical pain. The comorbidity of those pain hypersensitivity syndromes that present in the absence of inflammation or a neural lesion, their similar pattern of clinical presentation and response to centrally acting analgesics, may reflect a commonality of central sensitization to their pathophysiology. An important question that still needs to be determined is whether there are individuals with a higher inherited propensity for developing central sensitization than others, and if so, whether this conveys an increased risk in both developing conditions with pain hypersensitivity, and their chronification. Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. We have certainly come a long way since the first discovery of activity-dependent synaptic plasticity in the spinal cord and the revelation that it occurs and produces pain hypersensitivity in patients. Nevertheless, discovering the genetic and environmental contributors to and objective biomarkers of central sensitization will be highly beneficial, as will additional treatment options to prevent or reduce this prevalent and promiscuous form of pain plasticity.
In this article, the authors present evidence regarding a dissociative subtype of PTSD, with clinical and neurobiological features that can be distinguished from nondissociative PTSD. The dissociative subtype is characterized by overmodulation of affect, while the more common undermodulated type involves the predominance of reexperiencing and hyperarousal symptoms. This article focuses on the neural manifestations of the dissociative subtype in PTSD and compares it to those underlying the reexperiencing/hyperaroused subtype. A model that includes these two types of emotion dysregulation in PTSD is described. In this model, reexperiencing/hyperarousal reactivity is viewed as a form of emotion dysregulation that involves emotional undermodulation, mediated by failure of prefrontal inhibition of limbic regions. In contrast, the dissociative subtype of PTSD is described as a form of emotion dysregulation that involves emotional overmodulation mediated by midline prefrontal inhibition of the same limbic regions. Both types of modulation are involved in a dynamic interplay and lead to alternating symptom profiles in PTSD. These findings have important implications for treatment of PTSD, including the need to assess patients with PTSD for dissociative symptoms and to incorporate the treatment of dissociative symptoms into stage-oriented trauma treatment.
The long-term consequences of falanga are probably the best described consequences of exposure to specific forms of physical torture. Theories about casual lesions in the peripheral tissues of the feet have been put forward based on clinical observations along with international guidelines for the clinical assessment, but still knowledge is needed in several areas. A review of the literature on falanga is presented, mainly focusing on the clinical aspects and possible lesions caused by this specific form of torture that may influence the overall management of the condition. Finally, the article closes with a call for future research, which is needed in order to advance a knowledge-based development of the applied clinical practice.
One of the most distressing symptoms of pain syndromes is the enhanced pain sensation (hyperalgesia). Understanding the pathophysiology of hyperalgesia and the mode of action of antihyperalgesic drugs will potentially lead to better strategies in neuropathic pain therapy. In the present study we used fMRI in combination with quantitative sensory testing and explored brain activation patterns during acute impact pain and mechanical hyperalgesia in the human UV-B model. To gain insight into pharmacological modulation of pain and hyperalgesia, we investigated potential differential fMRI correlates of analgesic and antihyperalgesic effects of two intravenous cyclooxygenase (COX) inhibitors, i.e. parecoxib and acetylsalicylic acid (ASA). Fourteen healthy volunteers (mean age 27.4 years) participated in this double-blinded, randomized and placebo-controlled crossover study. Tactile stimuli and mechanical impact hyperalgesia were tested at the site of a UV-B irradiation and acute mechanical pain was tested at a site distant from the irradiated skin. These measurements were conducted before and 30 minutes after a 5 minutes lasting intravenous infusion of either saline (placebo), parecoxib 40mg or ASA 1000mg. During fMRI experiments, subjects were asked to rate the evoked pain sensations on a visual analogue scale. Acute mechanical pain and mechanical hyperalgesia led to widespread activations of brain areas known to comprise the human pain matrix. However, analgesic and antihyperalgesic drug effects differed substantially. Analgesic effects were found in primary and secondary somatosensory cortices and anterior parts of the cingulate gyrus. In contrast, antihyperalgesic effects were detected in primary somatosensory, parietal association and anterior cingulate cortex, but not in secondary somatosensory cortices. Therefore, we provide evidence for a differential modulation of brain areas under either analgesia and antihyperalgesia.
Supported by the German Research Network “Neuropathic Pain“ of the German Federal Ministry of Education and Research (Bundesministerium für Bildung und Forschung; BMBF)
To examine headache trajectories among persons with mild Traumatic Brain Injury (mTBI) in the year following injury, and the relationship of headache trajectory to PTSD at one year post injury.
Prospective, Longitudinal study SETTING: Participants were recruited through a university medical center and participated in follow-up assessments by telephone.
212 prospectively enrolled individuals within one week of mTBI who were hospitalized for observation or other system injuries. Participants were assessed at baseline, three, six, and twelve months post-injury.
Not applicable MAIN OUTCOME MEASURES: Participants rated average headache pain intensity using the 0-10 numeric rating scale at each assessment period. The PTSD Checklist - Civilian Version (PCL-C) was completed at twelve months post-injury.
Latent Class Growth Analysis produced a four trajectory group model, with groups labeled Resolved, Worsening, Improving, and Chronic. Multivariate regression modeling revealed that younger age and premorbid headache correlated with membership in worse trajectory groups (Worsening and Chronic; p<.001). Univariate regression revealed a significant association between PTSD and membership in worse trajectory groups (p<.001).
Headache is common in the year following mTBI, with younger people, persons who previously had headaches, and persons with PTSD more likely to report Chronic or Worsening headache. Further research is needed to examine whether PTSD symptoms exacerbate headaches, or whether problematic headache symptoms exacerbate PTSD.
Copyright © 2015 American Congress of Rehabilitation Medicine. Published by Elsevier Inc. All rights reserved.
Posttraumatic stress disorder (PTSD) and chronic pain often co-occur and exacerbate each other. Elucidating the mechanism of this co-occurrence therefore has clinical importance. Previously, PTSD patients with chronic pain were found to demonstrate a unique, paradoxical pain profile: hyper-responsiveness together with hyposensitivity to pain. Our aim was to examine whether two seemingly paradoxical facets of PTSD - anxiety and dissociation - underlie this paradoxical profile. PTSD patients (n=32) and healthy controls (n=43) underwent psychophysical testing and completed questionnaires. PTSD patients had higher pain thresholds and higher pain ratings to suprathreshold stimuli than controls. Pain thresholds were positively associated with dissociation levels and negatively associated with anxiety sensitivity levels. Experimental pain ratings were positively associated with anxiety sensitivity and negatively related to dissociation levels. Chronic pain intensity was associated with anxiety, anxiety sensitivity and pain catastrophizing. It appears that reduced conscious attention towards incoming stimuli, resulting from dissociation, causes delayed response in pain threshold measurement while biases towards threatening stimuli and decreased inhibition, possibly due to elevated anxiety, are responsible for the intensification of experimental and chronic pain. The paradoxical facets of PTSD and their particular influences over pain perception seem to reinforce the coexistence of PTSD and chronic pain, and should be considered when treating traumatized individuals.
This article provides new information regarding the underlying mechanism of the coexistence of PTSD and chronic pain. This knowledge could potentially help to provide better management of PTSD and chronic pain among individuals in the aftermath of trauma.
Copyright © 2015 American Pain Society. Published by Elsevier Inc. All rights reserved.
Background
Stress-induced dissociative states involving analgesia are a common feature of borderline personality disorder (BPD) and posttraumatic stress disorder (PTSD). Our aim was to investigate the psychologic, somatosensory (pain sensitivity) and neural correlates of dissociative states in patients with these disorders.
While longitudinal posttraumatic stress responses are known to be heterogeneous, little is known about predictors of those responses. We investigated if locus of control (LOC) and coping style are associated with long-term PTSD-trajectories after exposure to combat. Six hundred and seventy five Israeli soldiers with or without combat stress reaction (CSR) from the Lebanon war were assessed 1, 2, and 20 years after the war. Combat exposure, LOC, and coping style were then investigated as covariates of the trajectories of resilience, recovery, delayed onset, and chronicity. Symptomatic trajectories in the CSR and the non-CSR group were significantly associated to varying degrees with perceived life threat during combat (ORs: 1.76-2.53), internal LOC (0.77-0.87), emotional coping style (0.28-0.34), and low use of problem-focused coping (2.12-3.11). In conclusion, assessment of LOC and coping can aid prediction of chronic PTSD outcomes of combat exposure.
Copyright © 2015 Elsevier Ltd. All rights reserved.
Psychological trauma is associated with an increased risk for chronification of nonspecific chronic back pain (nsCLBP) independent of posttraumatic stress disorder (PTSD). However, the mechanisms underlying the role of psychological trauma in nsCLBP are less clear than in PTSD. Therefore, this study considered whether psychological trauma exposure (TE) is accompanied by specific alterations in pain perception. The study included 56 participants with nsCLBP and TE (nsCLBP-TE), 93 participants with nsCLBP without TE (nsCLBP-W-TE), and 31 pain-free controls. All participants underwent a thorough clinical evaluation. The standardized quantitative sensory testing protocol of the "German Research Network on Neuropathic Pain" was used to obtain comprehensive profiles on somatosensory functions in painful (back) and non-painful areas (hand). The protocol consisted of thermal and mechanical detection as well as pain thresholds, vibration thresholds, and pain sensitivity to sharp and blunt mechanical stimuli. Psychological trauma was validated by structured clinical interview. Trauma-associated symptom severity, anxiety, and depressive symptomatology were assessed by self-report questionnaires. Differences in somatosensory function were seen only for pressure pain thresholds. Compared with controls, nsCLBP-TE revealed hyperalgesia generalized in space with lower thresholds in painful and non-painful areas, whereas nsCLBP-W-TE demonstrated localized alterations with decreased thresholds only in the pain-affected area of the back (P ≤ 0.006). Our findings suggest an augmented central pain processing in nsCLBP-TE (alterations in painful and non-painful areas), whereas nsCLBP-W-TE show only local changes (alterations only in the painful area) suggesting regional sensitization processes. This finding might explain why TE without PTSD is associated with an increased prevalence of chronic pain.
The bed nucleus of the stria terminalis (BNST) is an important relay for multiple cortical and subcortical regions involved in processing anxiety as well as neuroendocrine and autonomic responses to stress, and it is thought to play a role in the dysregulation of these functions as well as in addictive behavior. While its architecture and connection profile have been thoroughly examined in animals, studies in humans have been limited to post-mortem histological descriptions of the BNST itself, not accounting for the distribution of its various connections. In the current study, we used diffusion-weighted magnetic resonance imaging (DW-MRI) to investigate the courses of fiber tracks connected to the BNST in humans. We restricted our seed region for probabilistic fiber tracking to the dorsal part of the BNST, as the ventral BNST is not distinguishable from the surrounding grey matter structures using magnetic resonance imaging. Our results show two distinct pathways of the BNST to the amygdala via the stria terminalis and the ansa peduncularis, as well as connections to the hypothalamus. Finally, we distinguished a route to the orbitofrontal cortex (OFC) running through the head of the caudate nucleus (CN) and the nucleus accumbens (NAcc). Pathways to brainstem regions were found to show a considerable inter-individual variability and thus no common pathway could be identified across participants. In summary, our findings reveal a complex network of brain structures involved in behavioral and neuroendocrine regulation, with the BNST in a central position.
Copyright © 2015 Elsevier Ltd. All rights reserved.
Chronic pain is an important public health problem that negatively impacts quality of life of affected individuals and exacts an enormous socio-economic cost. Currently available therapeutics provide inadequate management of pain in many patients. Acute pain states generally resolve in most patients. However, for reasons that are poorly understood, in some individuals, acute pain can transform to a chronic state. Our understanding of the risk factors that underlie the development of chronic pain is limited. Recent studies have suggested an important contribution of dysfunction in descending pain modulatory circuits to pain 'chronification'. Human studies provide insights into possible endogenous and exogenous factors that may promote the conversion of pain into a chronic condition.
Descending pain modulatory systems have been studied and characterized in animal models. Human brain imaging techniques, deep brain stimulation and the mechanisms of action of drugs that are effective in the treatment of pain confirm the clinical relevance of top-down pain modulatory circuits. Growing evidence supports the concept that chronic pain is associated with a dysregulation in descending pain modulation. Disruption of the balance of descending modulatory circuits to favour facilitation may promote and maintain chronic pain. Recent findings suggest that diminished descending inhibition is likely to be an important element in determining whether pain may become chronic. This view is consistent with the clinical success of drugs that enhance spinal noradrenergic activity, such as serotonin/norepinephrine reuptake inhibitors (SNRIs), in the treatment of chronic pain states. Consistent with this concept, a robust descending inhibitory system may be normally engaged to protect against the development of chronic pain. Imaging studies show that higher cortical and subcortical centres that govern emotional, motivational and cognitive processes communicate directly with descending pain modulatory circuits providing a mechanistic basis to explain how exogenous factors can influence the expression of chronic pain in a susceptible individual.
Preclinical studies coupled with clinical pharmacologic and neuroimaging investigations have advanced our understanding of brain circuits that modulate pain. Descending pain facilitatory and inhibitory circuits arising ultimately in the brainstem provide mechanisms that can be engaged to promote or protect against pain 'chronification'. These systems interact with higher centres, thus providing a means through which exogenous factors can influence the risk of pain chronification. A greater understanding of the role of descending pain modulation can lead to novel therapeutic directions aimed at normalizing aberrant processes that can lead to chronic pain.
Background
Post-traumatic stress disorder (PTSD) and pain have a well-documented high comorbidity; however, the underlying mechanisms of this comorbidity are currently poorly understood. The aim of this psychophysical study was to investigate the behavioral response to a prolonged suprathreshold pain stimulus in subjects with combat-related PTSD and combat controls (CC) for clinical evidence of central sensitization.Methods
Ten male subjects with current PTSD related to combat and 11 CC male subjects underwent baseline quantitative sensory testing (QST), temporal pain summation, and psychological profiling followed by an intramuscular injection of capsaicin into the quadriceps muscle.ResultsThere was no significant between-group difference for the initial maximal pain response or an initial pain reduction for the first 15 minutes postinjection on QST or pain ratings. However, we observed significantly higher scores in the PTSD group for the second 15 minutes postinjection on both pain intensity and pain unpleasantness ratings. Assessment of temporal summation to repetitive pressure stimuli showed significantly higher subjective pain in the PTSD group.Conclusion
These findings are consistent with a significantly higher degree of acute central sensitization in individuals with PTSD. Increased acute central sensitization may underlie increased vulnerability for developing pain-related conditions following combat trauma.
Tissue injury may, in some instances, induce chronic pain lasting for decades. Torture survivors suffer from high rates of chronic pain and hypersensitivity in the previously injured regions. Whether torture survivors display generalized alterations in pain perception and modulation, and whether such alterations underlie their chronic pain is unknown. We aimed at exploring the long-term alterations in pain perception and modulation in torture survivors.
In order to address these questions, a systematic quantitative somatosensory evaluation was performed in individuals (n = 60) who suffer from chronic pain, and who, decades previously, were tortured, resulting in substantial tissue damage. These individuals were compared with age- and sex-matched individuals (n = 44) of similar background. Testing included the measurement of pain threshold and pain tolerance, perceived suprathreshold stimuli, conditioned pain modulation (CPM) and temporal summation of pain (TSP) in intact body regions.
Chronic pain was found highly prevalent (86.6%) among torture survivors, who exhibited higher suprathreshold pain ratings (p < 0.05), poorer CPM (p < 0.0001) and stronger TSP (p < 0.0001) than controls. Significant differences in CPM and TSP were also found between torture survivors and controls with chronic pain. Chronic pain intensity among torture survivors correlated negatively with the magnitude of CPM (r = -0.47, p < 0.01).
Torture appears to induce generalized dysfunctional pain modulation that may underlie the intense chronic pain experienced by torture survivors decades after torture. The results may be generalized to instances where chronic pain exists for decades after severe injury in non-tortured populations and emphasize the importance of preventive care.
An increased vulnerability to pain complaints, along with a simultaneous increase in experimental pain thresholds, shows the paradoxical phenomenon of pain perception in depressive patients. Clomipramine, a tricyclic antidepressant, could also ameliorate syndromes in chronic pain patients. However, few studies have focused on the effect of antidepressants on experimental pain thresholds. By using a rat model, the learned helplessness paradigm, the present study explored the effect of clomipramine on behavioral deficits and experimental pain thresholds to different stimuli in "helpless" rats. Helpless rats were administered clomipramine (10mg/kg, i.p, b.i.d.) for 5 consecutive days. The depressive-like and anxiety-like behaviors were detected by shuttle box, open field and elevated plus maze test before and after inescapable shock and after medication. The sensitivity to the thermal and mechanical stimuli was also measured by the von Frey hair and Hargreaves test at the indicated time points. Helpless rats displayed shorter total travel distance and fewer rearing times in the open field test and decreased percentage of time spent in the open arms in the elevated plus maze test. In addition, they exhibited significant hypoalgesia/hypoesthesia to mechanical and thermal stimuli. Clomipramine alleviate depressive-like and anxiety-like behaviors and increased the sensitivity to von Frey filament stimuli with no effect on the sensitivity to radiant heat stimuli in helpless rats. These suggested that clomipramine could reverse mechanical but not thermal hypoalgesia/hypoesthesia and simultaneously improved behavioral deficits.
People with chronic pain and comorbid posttraumatic stress disorder (PTSD) report more severe pain and poorer quality of life than those with chronic pain alone. This study evaluated the extent to which associations between PTSD and chronic pain interference and severity are mediated by pain-related coping strategies and depressive symptoms. Veterans with chronic pain were divided into 2 groups, those with (n=65) and those without (n=136) concurrent PTSD. All participants completed measures of pain severity, interference, emotional functioning, and coping strategies. Those with current PTSD reported significantly greater pain severity and pain interference, had more symptoms of depression, and were more likely to meet diagnostic criteria for a current alcohol or substance use disorder (all p-values <.01). Participants with PTSD reported more use of several coping strategies, including guarding, resting, relaxation, exercise/stretching, and coping self-statements. Illness-focused pain coping (i.e., guarding, resting, and asking for assistance) and depressive symptoms jointly mediated the relationship between PTSD and both pain interference (total indirect effect=0.194, p<.001) and pain severity (total indirect effect=0.153, p=.004). Illness-focused pain coping also evidenced specific mediating effects, independent of depression. In summary, specific pain coping strategies and depressive symptoms partially mediated the relationship between PTSD and both pain interference and severity. Future research should examine whether changes in types of coping strategies after targeted treatments predict improvements in pain-related function for chronic pain patients with concurrent PTSD.
The human startle response is modulated by emotional experiences, with startle potentiation associated with negative affect. We used positron emission tomography with 15O-water to study neural networks associated with startle modulation by phobic fear in a group of subjects with specific snake or spider phobia, but not both, during exposure to pictures of their feared and non-feared objects, paired and unpaired with acoustic startle stimuli. Measurement of eye electromyographic activity confirmed startle potentiation during the phobic as compared with the non-phobic condition. Employing a factorial design, we evaluated brain correlates of startle modulation as the interaction between startle and affect, using the double subtraction contrast (phobic startle vs. phobic alone) vs. (non-phobic startle vs. non-phobic alone). As a result of startle potentiation, a significant increase in regional cerebral blood flow was found in the left amygdaloid–hippocampal region, and medially in the affective division of the anterior cingulate cortex (ACC). These results provide evidence from functional brain imaging for a modulatory role of the amygdaloid complex on startle reactions in humans. They also point to the involvement of the affective ACC in the processing of startle stimuli during emotionally aversive experiences. The co-activation of these areas may reflect increased attention to fear-relevant stimuli. Thus, we suggest that the amygdaloid area and the ACC form part of a neural system dedicated to attention and orientation to danger, and that this network modulates startle during negative affect.
The purpose of this study was to assess differences in beliefs about pain and coping strategies employed in veterans with comorbid chronic pain and posttraumatic stress disorder (PTSD), compared to veterans with chronic pain alone. It was hypothesized that veterans with comorbid chronic pain and significant levels of PTSD symptomatology would report higher levels of maladaptive coping strategies and beliefs about pain when compared to veterans with pain alone.
Data were obtained from 194 veterans who completed self-report questionnaires as part of their participation in a Psychology Pain Management Program at a northeastern Department of Veterans Affairs healthcare facility.
Analyses indicated that 47.4% of the sample scored above the clinical cutoff for PTSD symptomatology on the PTSD Checklist - Military Version (PCL-M). A Multivariate Analysis of Covariance (MANCOVA) was conducted with age and pain intensity as covariates. In support of the hypothesis, veterans with comorbid chronic pain and significant levels of PTSD symptomatology endorsed significantly higher levels of maladaptive coping strategies and beliefs about pain (greater catastrophizing and emotional impact on pain; less control over pain) when compared to veterans with chronic pain alone.
The results of this study suggest potential explanations for the previously observed negative effect of PTSD on chronic pain. Moreover, the results suggest specific targets for intervention with patients who have comorbid pain and PTSD.
This review deals with physiological and biological mechanisms of neuropathic pain, that is, pain induced by injury or disease of the nervous system. Animal models of neuropathic pain mostly use injury to a peripheral nerve, therefore, our focus is on results from nerve injury models. To make sure that the nerve injury models are related to pain, the behavior was assessed of animals following nerve injury, i.e. partial/total nerve transection/ligation or chronic nerve constriction. The following behaviors observed in such animals are considered to indicate pain: (a) autotomy, i.e. self-attack, assessed by counting the number of wounds implied, (b) hyperalgesia, i.e. strong withdrawal responses to a moderate heat stimulus, (c) allodynia, i.e. withdrawal in response to non-noxious tactile or cold stimuli. These behavioral parameters have been exploited to study the pharmacology and modulation of neuropathic pain. Nerve fibers develop abnormal ectopic excitability at or near the site of nerve injury. The
The periaqueductal gray matter (PAG), a known modulator of somatic pain transmission, shows evidence of interictal functional and structural abnormalities in migraineurs, which may contribute to hyperexcitability along spinal and trigeminal nociceptive pathways, and lead to the migraine attack. The aim of this study was to examine functional connectivity of the PAG in migraine.
Using resting-state functional MRI, we compared functional connectivity between PAG and a subset of brain areas involved in nociceptive/somatosensory processing and pain modulation in 17 subjects with migraine, during a pain-free state, versus 17 gender- and age-matched controls. We also assessed the relation between intrinsic resting-state correlations within PAG networks and the average monthly frequency of migraine attacks, as well as allodynia.
Our findings show stronger connectivity between the PAG and several brain areas within nociceptive and somatosensory processing pathways in migraineurs versus controls. In addition, as the monthly frequency of migraine attacks worsens, the strength of the connectivity in some areas within these pathways increases, whereas a significant decrease in functional resting-state connectivity between the PAG and brain regions with a predominant role in pain modulation (prefrontal cortex, anterior cingulate, amygdala) can be evidenced. Finally, migraineurs with a history of allodynia exhibit significantly reduced connectivity between PAG, prefrontal regions, and anterior cingulate compared to migraineurs without allodynia.
These data reveal interictal dysfunctional dynamics within pain pathways in migraine manifested as an impairment of the descending pain modulatory circuits, likely leading to loss of pain inhibition, and hyperexcitability primarily in nociceptive areas.
Uncontrollable stress is frequently accompanied by a primarily opioid-mediated stress analgesia. In posttraumatic stress disorder (PTSD) exaggerated stress-induced analgesia to trauma reminders was proposed. The present study investigated whether enhanced analgesia occurs in response to a trauma-unrelated cognitive stressor in PTSD.
Functional magnetic resonance imaging data were obtained from fourteen outpatients with PTSD and 14 trauma-exposed subjects without PTSD (NPTSD) during mechanical painful stimulation before and after stress. Blood oxygenation level-dependent (BOLD) responses were assessed during painful stimulation. Pain ratings, pain thresholds and pain tolerance were assessed pre- and post-stress. Heart rate and blood pressure were recorded before, during and after stress.
In comparison to NPTSD, PTSD-patients showed significantly more analgesia in terms of an increase of pain threshold and tolerance and a decrease in pain ratings after the stressor. Post-stress, PTSD-patients compared to NPTSD displayed more activation of the rostral anterior cingulate cortex and decreased neural activity in brain areas associated with pain perception. However heart rate increase during stress and blood pressure decrease post-stress was lower in PTSD pointing to a dysregulation of the cardiovascular system in response to stress.
The small sample size represents a limiting factor in interpreting the results and might have led to low levels of significance for the group differences in BOLD response changes.
These findings show enhanced stress reactivity and accompanying reduced pain perception in PTSD-patients in contrast to traumatized participants without PTSD. The results suggest that the previously reported enhanced analgesic response after trauma-related stress in PTSD transfers to trauma-unrelated stressors.
Pain and Post Traumatic Stress Disorder (PTSD) are highly comorbid conditions. Patients with chronic pain have higher rates of PTSD. Likewise, patients with PTSD are often diagnosed with numerous chronic pain conditions. Despite the high pain-PTSD comorbidity, the neurobehavioral mechanisms underlying this phenomenon are incompletely understood and only recently researchers have started investigating it using experimental models. In this article, we systematically review the substantial clinical evidence on the co-occurrence of pain and PTSD, and the limited experimental evidence of pain processing in this disorder. We provide a detailed overview of the psychophysical and brain imaging experiments that compared somatosensory and pain processing in PTSD and non-PTSD populations. Based on the presented evidence, an extensive body of literature substantiates the clinical coexistence of pain and PTSD in patients but the limited experimental data show inconsistent results highlighting the need for well-controlled future studies. This article is part of a Special Issue entitled 'Post-Traumatic Stress Disorder'.
Previous studies reported increased heat pain thresholds and decreased ischemic pain thresholds in patients experiencing depression. The increased sensitivity to ischemic muscle pain was assumed to represent a model for the investigation of physical symptoms in the disease. Here, we explored how the serotonin and noradrenaline reuptake inhibitor duloxetine influences experimental pain thresholds and tolerances in depressed patients during treatment. Twenty-two patients experiencing unipolar depression were included. Pain assessments were conducted unmedicated at baseline, after 1 week, and after 6 weeks of duloxetine treatment. We observed the expected clinical response of patients indicated by a significant reduction in the Montgomery Depression Rating Scale after 6 weeks. At baseline, we found increased heat pain thresholds in patients in comparison to controls while patients simultaneously rated augmented pain perception on the visual analog scale. In contrast, patients were significantly more perceptive to ischemic muscle pain at baseline. During treatment, the examined pain thresholds showed differential changes: Increased heat pain thresholds of patients normalized during treatment, whereas no significant change was observed for ischemic pain thresholds. Thus, our results might change the view on the paradox of pain perception in major depression because increased heat pain thresholds are associated with augmented pain perception in the disease.
The present prospective longitudinal study on chronic postoperative pain was conducted to assess the predictive power of attentional and emotional variables specifically assumed to augment pain, such as pain hypervigilance, pain-related anxiety, pain catastrophizing and attentional biases to pain. Their relevance was determined in comparison with other psychological and physiological predictors (depression, anxiety, somatization, cortisol reactivity, pain sensitivity). In 84 young male patients the predictor variables were assessed one day before surgery (correction of chest malformation). Postoperative outcome (subjective pain intensity and pain-related disability) was assessed three (N=84) and six months (N=78) after surgery. Patients were classified into good and poor outcome groups. Patients with high pain intensity three (25%) or six months (14%) after surgery, differed significantly from those low in pain with regard to their preoperative performance in the dot-probe task (high attentional bias towards positive words). A sizeable portion (54%) of patients still felt disabled due to pain after three months and a few patients after six months (13%). These patients were those with high preoperative ratings in the Pain Vigilance and Awareness Questionnaire. The few subjectively disabled patients after six months could be identified in addition by low pressure pain and high cold pain thresholds before surgery. An attentional bias towards positive stimuli prior to surgery may indicate a maladaptive coping style, which avoids necessary confrontation with pain and predisposes patients to chronic postoperative pain. Lasting subjectively felt pain-related disability occurs predominantly in patients with high levels of pain hypervigilance before surgery.
The ability of a painful stimulus to suppress pain in another, remote area (DNIC) has been intensely studied. However, the effect of the distance between the two painful stimuli and the attentional factors during the measurement of pain perception received minimal treatment. We evaluated the effect of these factors on DNIC and on the interaction between DNIC and spatial summation (SS) of pain. Subjects rated the intensity of a test stimulus (applied to one hand) alone and simultaneously with conditioning stimuli applied to four different locations; 5 and 30cm from the test stimulus on the same hand, the contralateral hand and contralateral leg. In each location, ratings were performed under three different instructions: summation, attention to test stimulus, attention to conditioning stimulus. The distance between the conditioning and test stimulus significantly affected pain perception (p<0.01) regardless of the instructions; SS occurred only at a distance of 5cm and DNIC occurred only in the remaining distances. DNIC's magnitude increased as the distance between the two stimuli increased (p<0.01). However, the instruction to summate attenuated DNIC and the DNIC instruction attenuated SS of pain. Attention to the conditioning stimulus induced a stronger DNIC than attention to the test stimulus (p<0.001). We conclude that (1) DNIC and SS of pain appear to be antagonistic processes. (2) DNIC is affected by the distance between two noxious stimuli and to a lesser extent, by attention. (3) The interaction between DNIC, SS and attention is complex and reflects the role of sensory-cognitive integration in pain perception.
Refugee survivors of torture in the United Kingdom have multiple problems, of which pain may be underrecognized, given the high prevalence recorded in similar populations in Denmark.
To establish in a UK sample the prevalence of persistent pain and to investigate associations between specific pains and torture methods.
A cohort of a random 20% sample attending a specialist UK center for survivors of torture in 2005 was taken. All complaints of pain recorded at initial interview were categorized for body site and putative pain mechanism. These were compared with the database of personal variables and data on torture using odds ratios (ORs) and exact probability.
Of 115 men and 63 women, with mean age of 30 years, 78% reported persistent multiple pains, mainly in the head and low back. They had experienced a median of six torture methods. There was a clear association between female abdominal/pelvic/genital pain and rape/sexual assault (17 of 34 vs. zero of 17: exact P<0.001) and between male anal pain and rape (two of nine vs. two of 77: OR=6.00; 95% confidence interval=1.79-20). Tests of foot/leg pain with falaka and shoulder pain with suspension did not show expected associations.
A significant relationship emerged between torture and report of persistent pain at a high prevalence. Findings do not support the widespread clinical assumption that complaint of persistent pain after torture is predominantly a manifestation of psychological distress. Rather, complaints of pain in torture survivors should be assessed and treated in relation to physical trauma.
Intimate partner violence (IPV) is one of the most common causes of posttraumatic stress disorder (PTSD) in women. Women with IPV-related PTSD often experience comorbid chronic pain and pain-related disability. Despite the high comorbidity between PTSD and chronic pain, recent evidence suggests that male veterans with combat-related PTSD report decreased sensitivity to experimental pain. The aim of this study was to examine the neurobehavioral correlates of experimental pain in women with IPV-related PTSD.
Functional magnetic resonance neuroimaging data were collected during an event-related experimental pain paradigm that was administered twice to 23 women with IPV-related PTSD and 15 age-, race- and education-comparable nontraumatized control women. Brief thermal heat stimuli were repeatedly applied to the left volar forearm, and subjects rated the perceived temperature intensity with a button-box.
Women with IPV-related PTSD relative to nontraumatized control women showed: 1) increased activation of right middle insula and right dorsolateral prefrontal cortex during initial painful stimulation, and 2) subsequent decrease in subjective intensity ratings with repeated exposure to pain, which was accompanied by attenuation of activation within right anterior insula that was associated with avoidance symptoms of PTSD.
These results suggest that women with IPV-related PTSD show dysregulated functional brain activity during pain processing, which might drive maladaptive coping mechanisms, such as avoidance and numbing.
There is a growing body of knowledge on pain modulation in various disease states. This article reviews the state of the art regarding the clinical relevance of pain inhibition as revealed by 'pain inhibits pain' test paradigms, trying to organize the clinically relevant data, and emphasizing the pathophysiology of pain. In line with recent experts' recommendations, the term conditioned pain modulation (CPM) will be used, replacing the previous terms 'diffuse noxious inhibitory control (DNIC)' or 'DNIC-like' effects.
Most of the work in this context was done on the idiopathic pain syndromes, such as irritable bowel syndrome, temporomandibular disorders, fibromyalgia, and tension type headache. The pattern of reduced CPM efficiency seems common to these syndromes and an assertion is made that low CPM efficiency, reflecting low pain inhibitory capacity, is a pathogenetic factor in the development of the idiopathic pain syndromes. Low CPM efficiency was shown to be predictive of acute and chronic postoperative pain, and, in some reports, to be associated with neuropathic pain levels.
Low CPM efficiency is associated with higher pain morbidity and vice versa. Further work is awaited on clarifying plasticity of CPM and its relevance to selection and efficacy of pain therapy.
To describe activity limitations in tortured refugees referred for rehabilitation, particularly the impact of neuropathic pain resulting from falanga (beatings under the feet).
Physiotherapists assessed 103 consecutively referred torture victims with a long history of sequelae, among them pain and mobility problems. All had been subjected to various forms of physical and psychological torture and 71 victims had also suffered falanga. Main outcome measures used were: the Disability Rating Index (DRI; 12 items) to assess self-reported capacity to carry out daily activities; for falanga victims, a specific foot assessment of sensory function in the feet.
All patients perceived clear activity limitations according to the DRI. The falanga victims' feet were categorised according to the type of foot pain: stimulus-independent pain; stimulus-evoked pain; no pain. The two groups with foot pain displayed sensory dysfunction and suffered more extensive activity limitations. After correction for confounding factors, these two groups reported significantly more activity limitations in 7 out of 12 DRI items than those who were not exposed to falanga.
In this group of victims who had chronic pain for at least 5 years after torture, all perceived activity limitations, but pain from falanga had a greater overall impact on disability assessed in terms of daily activities.
Torture is widely practiced throughout the world. Recent studies indicate that 50% of all countries, including 79% of the G-20 countries, continue to practice systematic torture despite a universal ban. It is well known that torture has numerous physical, psychological, and pain-related sequelae that can inflict a devastating and enduring burden on its victims. Health care professionals, particularly those who specialize in the treatment of chronic pain, have an obligation to better understand the physical and psychological effects of torture. This review highlights the epidemiology, classification, pain sequelae, and clinical treatment guidelines of torture victims. In addition, the role of pharmacologic and psychologic interventions is explored in the context of rehabilitation.
Stress-induced dissociative states involving analgesia are a common feature of borderline personality disorder (BPD) and posttraumatic stress disorder (PTSD). Our aim was to investigate the psychologic, somatosensory (pain sensitivity) and neural correlates of dissociative states in patients with these disorders.
We included 15 women with BPD who were not taking medication; 10 of these women had comorbid PTSD. While undergoing functional magnetic resonance imaging at 1.5 Tesla, participants were exposed to a script describing a personalized dissociation-inducing situation and a personalized script describing a neutral situation. We assessed dissociative psychopathology and pain sensitivity.
Dissociative psychopathology scores were significantly higher and pain sensitivity was lower after the dissociation-inducing script was read compared with the neutral script. The blood oxygen level-dependent (BOLD) signal was significantly increased in the left inferior frontal gyrus (Brodmann area [BA] 9) during the presentation of the dissociation-inducing script. Regression analyses revealed positive correlations between BOLD signal and dissociative psychopathology in the left superior frontal gyrus (BA 6) and negative correlations in the right middle (BA 21) and inferior temporal gyrus (BA 20). In the subgroup of participants with comorbid PTSD, we also found increased activity in the left cingulate gyrus (BA 32) during script-driven imagery-induced dissociation, a positive correlation between dissociation scores and activity in the right and left insula (BA 13) and a negative correlation in the right parahippocampal gyrus (BA 35).
The main limitation of this pilot study is the absence of a control group. Therefore, the results may also reflect the neural correlates of non-BPD/PTSD specific dissociative states or the neural correlates of emotionally stressful or "loaded" memories. Another limitation is the uncorrected statistical level of the functional magnetic resonance imaging results.
Our results showed that the script-driven imagery method is capable of inducing dissociative states in participants with BPD with and without comorbid PTSD. These states were characterized by reduced pain sensitivity and a frontolimbic activation pattern, which resembles the findings in participants with PTSD while in dissociative states.
Depressed mood alters the pain experience. Yet, despite its clear clinical relevance, little is known about the cognitive and neural mechanisms underlying this phenomenon. We tested an experimental manipulation to unravel the interaction between depressed mood and pain. We hypothesized that dysregulation of the neural circuitry underlying emotion regulation is the mechanism whereby pain processing is affected during depressed mood.
Using functional magnetic resonance imaging, we compared the effects of sad and neutral cognitive mood inductions on affective pain ratings, pain-specific cognitions, and central pain processing of a tonic noxious heat stimulus in 20 healthy volunteers.
The increase in negative pain-specific cognitions during depressed mood predicted the perceived increase in pain unpleasantness. Following depressed mood induction, brain responses to noxious thermal stimuli were characterized by increased activity in a broad network including prefrontal areas, subgenual anterior cingulate cortex, and hippocampus, as well as significantly less deactivation when compared with pain responses in a neutral mood. The participants who reported the largest increase in pain unpleasantness after the sad mood induction showed greater inferior frontal gyrus and amygdala activation, linking changes in emotion regulation mechanisms with enhancement of pain affect.
Our results inform how depressed mood and chronic pain co-occur clinically and may serve to develop and translate effective interventions using pharmacological or psychological treatment.
Several studies revealed reduced pain sensitivity in patients suffering from borderline personality disorder (BPD) under baseline and stress conditions. To establish whether these findings are specific for BPD, we compared pain thresholds in patients with BPD, posttraumatic stress disorder (PTSD), bulimia nervosa, and healthy controls.
The study included 76 female subjects: 16 patients with BPD, 16 patients with PTSD, 20 patients with bulimia nervosa and 24 healthy controls. Heat and cold pain thresholds were assessed under baseline and stress conditions, using a contact thermode. Mental stress was induced by the Paced Auditory Serial Addition Task.
Under baseline conditions, pain thresholds in patients with BPD were significantly higher compared to healthy controls. Patients with PTSD and bulimia nervosa did not show significant differences in pain thresholds compared to healthy controls. Under stress conditions, the difference between BPD patients and healthy controls became even more prominent, whereas the results in the other patient groups remained insignificant.
Our results support the hypothesis that reduced pain sensitivity is a prominent feature of BPD, which may differentiate this disorder from other stress-related psychiatric conditions.
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Altered function of endogenous pain modulation has been proposed as a mechanism that may underlie chronic pain conditions. Descending modulation of pain can be examined by diffuse noxious inhibitory controls (DNIC). DNIC comprises a spinal-medullary-spinal pathway that is activated when 2 concomitant painful stimuli are applied at the same time. This pain-inhibitory system can be easily triggered in an experimental setting. Therefore, studies on DNIC can help us to evaluate impairments in descending pain modulation, presumably primarily of inhibitory nature. This review summarizes recent findings on human DNIC trials with a specific focus on sex, age, and ethnic differences in DNIC effects and psychological mediators such as attention, expectation, and pain catastrophizing. Furthermore, the clinical relevance of DNIC studies will be discussed. Different methodological approaches used make it difficult to generalize results, but the research to date has shown good potential for DNIC to help in gaining insights in the underlying mechanisms of chronic pain conditions.
Perspective:
Recent literature on diffuse noxious inhibitory controls as a model of endogenous pain modulation in clinical pain syndromes was reviewed. DNIC may help to identify patients at risk for development of chronic pain and may open alternatives for treatment options.
The relationship between acute stress disorder (ASD), posttraumatic stress disorder symptoms (PTSD), and chronic pain was investigated in a longitudinal study of injured accident victims (N = 323, 64.7% men). Assessments took place 5 days (T1), 6 (T2) months, and 12 (T3) months postaccident. Relations between pain and posttraumatic stress symptoms were tested by structural equation modeling. Subjects diagnosed with full or subsyndromal PTSD at T2 and at T3 (14 and 19%) reported significantly higher pain intensity. Cross-lagged panel analysis yielded a mutual maintenance of pain intensity and ASD or PTSD symptoms across T2. Across the second half year, PTSD symptoms impacted significantly on pain but not vice versa. Clinicians need to pay careful attention to PTSD symptoms in accident survivors suffering from chronic pain.
The purpose of this article is to describe the current state-of-the-art regarding the co-occurrence of the anxiety disorders and chronic pain. First, we describe the core characteristics of chronic pain and its co-occurrence with the anxiety disorders. Second, we review data on the prevalence of co-occurrence. Third, we describe the mutual maintenance and shared vulnerability models, both of which have been offered to explain the co-occurrence of posttraumatic stress disorder (PTSD) and chronic pain and may have applicability to various other anxiety disorders. Fourth, we provide an integrative review of available research addressing the postulates of these models specific to the mechanisms of anxiety sensitivity, selective attention to threat, and reduced threshold for alarm. We conclude with general recommendations for improving assessment and treatment of patients who present with an anxiety disorder accompanied by clinically significant pain. Given that most of the available evidence has come from studies of PTSD and chronic pain, we provide a detailed agenda for future investigation of the co-occurrence of chronic pain and other anxiety disorders.
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Quantification of the human painful sensory experience is an essential step in the translation of knowledge from animal nociception to human pain. Translational models for assessment of pain are very important, as such models can be used in: 1) basic mechanistic studies in healthy volunteers; 2) clinical studies for diagnostic and monitoring purposes; 3) pharmacological studies to evaluate analgesic efficacy of new and existing compounds. Quantitative pain assessment, or quantitative sensory testing (QST), provides psychophysical methods that systematically document alterations and reorganization in nervous system function and, in particular, the nociceptive system. QST is defined as the determination of thresholds or stimulus response curves for sensory processing under normal and pathophysiological conditions. The modern concept of advanced QST for experimental pain assessment is a multimodality, multitissue approach where different pain modalities (thermal, mechanical, electrical, and chemical) are applied to different tissues (skin, muscles, and viscera) and the responses are assessed by psychophysical methods (thresholds and stimulus-response functions). Many new and advanced technologies have been developed to help relieve evoked, standardized, and painful reactions. Assessing pain has become a question of solving a multi-input, multi-output problem, with the solution providing the possibility of teasing out which pain pathways and mechanisms are involved, impaired, or affected.
Perspective:
Many methodologies have been developed for quantitative assessment of pain perception and involved mechanisms. This paper describes the background for the different methods, the use in basic pain experiments on healthy volunteers, how they can be applied in drug profiling, and the applications in clinical practice.