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Stressinduzierte Hyperalgesie (SIH) als Folge von emotionaler Deprivation und psychischer Traumatisierung in der Kindheit. Konsequenzen für die Schmerztherapie.
Abstract
It is now widely recognized that in many chronic pain syndromes the intensity and severity of individually perceived pain does not correlate consistently with the degree of peripheral nervous system tissue damage or with the intensity of primary afferent or spinal nociceptive neurone activity. In particular, stress and anxiety exert modulatory influences on pain depending on the nature, duration and intensity of the stressor and developmental influences on the maturation of the stress as well as the pain system. In some chronic pain syndromes, e. g. fibromyalgia, TMD or somatoform disorders, no nociceptive or neuropathic input is detectable. We summarise the studies investigating the neural substrates and neurobiological mechanisms of stressinduced hyperalgesia (SIH) in animals and humans. The review provides new perspectives and challenges for the current and future treatment of chronic pain.
... In bisherigen Arbeiten wurde vornehmlich der Zusammenhang mit dem Stressor belastender Kindheitserfahrungen für die anhaltende somatoforme Schmerzstörung (F45.40) oder das Fibromyalgiesyndrom diskutiert [5][4]) erfüllten. Zur Diagnosesicherung wurden im diagnostischen Prozess sowohl ursprünglich auslösende soma-tische Faktoren als auch begleitende psychische Faktoren identifiziert [17]. ...
... Es steht aber außer Frage, dass Zusammenhänge zwischen belastenden Kindheitserfahrungen und der Schmerzempfindlichkeit bei somatoformen Erkrankungen im engeren Sinne (F45.40) bestehen [5]. Interessant ist auch das Begleitresultat , dass fortschreitendes Alter mit einer erhöhten Schmerzsensibilität einherging . ...
... B. Noceboeffekt) mit beeinflusst werden und bilden nicht zwingenderweise eine peripher erniedrigte Schmerzschwelle ab [20]. Obwohl Stresserleben und Schmerzempfindlichkeit bekanntermaßen zusammenhängen und Schmerzempfindlichkeit ein anerkannter Modulator des Schmerzerlebens und seiner Aufrechterhaltung ist [5, 12, 18], ist die vorliegende Studie eine der ersten, die in einer Stichprobe von Schmerzpatienten gemäß F45.41 Zusammenhänge verschiedener lang anhaltender psychosozialer Stressoren direkt in Bezug auf die Schmerzempfindlichkeit untersucht und miteinander vergleicht. ...
BACKGROUND
Increased pain sensitivity is characteristic for patients with chronic pain disorder with somatic and psychological factors (F45.41). Persistent stress can induce, sustain, and intensify pain sensitivity, thereby modulating pain perception. In this context, it would be favorable to investigate which psychosocial stressors are empirically linked to pain sensitivity.
OBJECTIVES
The aim of this study was to examine the relationship between psychosocial stressors and pain sensitivity in a naturalistic sample of patients with chronic pain disorder with somatic and psychological factors (F45.41).
MATERIALS AND METHODS
We assessed 166 patients with chronic pain disorder with somatic and psychological factors (F45.41) at entry into an inpatient pain clinic. Pain sensitivity was measured with a pain provocation test (Algopeg) at the middle finger and earlobe. Stressors assessed were exposure to war experiences, adverse childhood experiences, illness-related inability to work, relationship problems, and potentially life-threatening accidents. Correlation analyses and structural equation modeling were used to examine which stressors showed the strongest prediction of pain sensitivity.
RESULTS
Patients exhibited generally heightened pain sensitivity. Both exposure to war and illness-related inability to work showed significant bivariate correlations with pain sensitivity. In addition to age, they also predicted a further increase in pain sensitivity in the structural equation model.
CONCLUSIONS
Bearing in mind the limitations of this cross-sectional study, these findings may contribute to a better understanding of the link between psychosocial stressors and pain sensitivity.
... wobei dies häufiger bei diffusen als bei gut lokalisierten Schmerzstörungen auftritt und meist mit einer reduzierten Schmerzschwelle einhergeht (Egle et al. 2016). Chronische Schmerzen werden folglich als biopsychosoziales Geschehen aufgefasst, bei dem neben «harten» biologischen Befunden, wie strukturellen oder entzündlichen Gewebeveränderungen, auch «weiche» psychosoziale Faktoren (sogenannte «yellow flags») eine Rolle spielen (Nicholas et al. 2011). ...
... Aufgrund von stressbedingten Einflüssen (z. B. Schmerz, Angst, Kälte u. a.) kann es zu einer Aktivierung des endogenen antinozizeptiven Systems und damit zu einer Schmerzhemmung kommen (Egle et al. 2016 (Dapunt et al 2018). Dies ist nicht zuletzt mit Blick auf den Einsatz von Analgetika wichtig. ...
... In human physiology, a complex interplay between an acute and chronic response to stress, hormonal regulation of homoeostasis, and neurotrophic factors exists. In human and animal studies, it has been shown that adverse childhood experiences (ACE) play a major role in the development of FSS and somatoform disorders [10,11] and are associated with susceptibility to painful conditions [12,13]. ...
... Through chronic stress, the allostatic overload of these systems leads to a static state of chronic overactivation as opposed to their natural dynamic adaptive response. The high prevalence of pain in patients with MSD due to higher leptin levels, as discussed above, is also plausible and could be one of the underlying mechanisms of stress-induced hyperalgesia often observed in patients with FSS and FMS [12]. ...
Objective:
Patients suffering from chronic pain often present with multifactorial underlying conditions, sometimes without concrete pathological physical findings. Functional somatic syndromes (FSS) and somatoform disorders show a high prevalence of 8-20% and are often associated with adverse childhood experiences (ACE) and chronic stress. As many different FSS have overlapping symptoms, the concept of multisomatoform disorder (MSD) has been introduced as an encompassing concept. We hypothesize that a common neurohumoral profile is present in patients with MSD that is distinct from gender- and age-matched controls and thus provides insight into possible common underlying mechanisms.
Design:
In 151 patients with MSD (138 females) and 149 matched controls (131 females), we determined ACE by the Childhood Trauma Questionnaire (CTQ) and chronic stress by the Trier Inventory for Chronic Stress (TICS). Furthermore, the serum levels of leptin, FSH, LH, cortisol, DHEA-S, and IGF-1 have been assessed.
Results:
There were significant differences in the levels of leptin, FSH, IGF-1, and cortisol between patients and controls, mainly driven by female participants. Levels of leptin were significantly correlated with BMI in patients, in controls, and in the female subgroup. This correlation was exaggerated in female patients when compared to female controls. Both CTQ and TICS predicted MSD directly and indirectly through the levels of leptin.
Conclusion:
There is evidence of a distinct neurohumoral profile in female patients with MSD when compared to matched healthy controls, similar to what has been demonstrated in other chronic pain states. The observed profile can be taken as possible evidence for a dysregulated response to chronic stress and metabolic balance as well as a state of hypocortisolism and HPA-axis dysfunction. ACE and chronic stress play a major role in the development of MSD and altered neurohumoral profile.
... Wir wissen, dass Migranten ein höheres Risiko für psychische Störungen haben (As sion 2004(As sion , 2005 und Flüchtlinge wiederum im Vergleich zu Migranten. Egle et al. (2016) weisen auch auf den Zusammenhang von lang anhaltenden Trennungssituationen und Ganzkörperschmerz hin. Auch der Zusammenhang zwischen einer posttraumatischen Belastungsstörung und chronischen Schmerzen ist hinlänglich beschrieben. ...
... ltungen» in der Bevölkerung und bei Ärzten, solche «Patientenkarrieren», wie der etwas zynisch anmutende Ausdruck heißt, keine Seltenheit. Wir haben wahrlich viel zu tun, ob in der ärztlichen Weiterbildung oder der Wissensvermittlung «nach außen», hin zu den Menschen! Entscheidend sind die klinischen Konsequenzen, die daraus gezogen werden sollten.Egle et al. (2016) fordern, dass bei chronischen Schmerzen ein möglicher biographischer Distress immer abgeklärt werden muss. Sie schlagen vor, für die durch Distress ausgelösten Mechanismen, die zu einem erhöhten Schmerzempfinden führen können, den von Grundlagenforschern (z. B. Imbe et al. 2006) eingeführten Begriff der stressinduzierten Hyperalgesie zu ...
Der folgende Beitrag beschäftigt sich mit verschieden Aspekten von Schmerz im Kontext psychiatrischer/psychosomatischer Behandlung. Eingangs wird auf die gesellschaftliche Kontextuierung von Schmerzen eingegangen, dann ein kurzer Blick auf den akuten Schmerz geworfen. Im Mittelpunkt steht der chronische Schmerz. Es werden dabei zunächst wichtige Aspekte zur Genese chronischer Schmerzen beleuchtet, anschließend werden klinische Implikationen besprochen. Abschließend wird auf psychodynamische Prozesse und Interaktionen in der Arzt/Therapeut-Patientenbeziehung im Rahmen der Schmerzbehandlung Bezug genommen.
... ). Chronischer Stress kann aufgrund eines erhöhten Cortisolspiegels zu toxischen Schädigungen in Amygdala, Hippocampus und vorderem Gyrus cinguli führen, d. h. in jenen Bereichen der zentralen Schmerzverarbeitung, die gleichzeitig auch für die Stressverarbeitung zuständig sind. Akuter Stress unterdrückt kurzfristig das Schmerzempfinden, chronischer Stress verstärkt es(Egle et al. 2016). Die vermehrte Cortisolausschüttung führt zusätzlich zu einer Schwächung der Immunabwehr und zu einer vermehrten Parodontitisaktivität. ...
Bruxismus und Myoarthropathie weisen komplexe Beschwerdebilder auf, in denen sowohl medizini sche als auch psychische Faktoren beteiligt sein können. Es wird aufgezeigt, wie Stress und die daraus folgenden muskulären Verspannungen auf die Beschwerdebilder einwirken und wie es zu einer Schmerzchronifizierung kommt. Anhand eines Stressmodells wird erklärt, wie Stress individuell verarbeitet wird und welche negativen Aus wirkungen dieser auf die Mundgesundheit und die Kieferfunktion hat. In der Diagnostik ist es dem Zahnarzt möglich, mittels eines ausführlichen Anamnesegesprächs und kurzen Testverfahrens, das Ausmass der Schmerzchronifizierung und der psychosozialen Belastung zu erfassen. Wenn nötig, soll der Zahnarzt die Patienten motivieren, eine psychologische Begleitung anzunehmen. In der Psychotherapie werden Schmerzbewälti gungsstrategien und Entspannungstechniken angewendet und der Umgang mit Schmerzen gelernt. Um einen langanhaltenden Behandlungs erfolg zu erzielen, müssen sowohl medizinische als auch psychosomatische Faktoren berücksichtigt werden.
... Die Schmerzerwartung ist insofern von der augenblicklichen biologischen, psychischen und sozialen Gesamtverfassung ebenso wie von vorausgegangenen Lernprozessen («perzeptives Gedächtnis») geprägt. Bei Letzteren können z.B. frühe Bindungsstörungen (in den ersten 18 Lebensmonaten) sowie körperliche Misshandlung und emotionale Deprivation in Kindheit und Jugend eine Rolle spielen, welche über epigenetische sowie psychoneuroendokrinologische und psychoneuroimmunologische (neuroinflammatorische) Mechanismen lebenslang zu einer dysfunktionalen Stress-und Schmerzverarbeitung führen können [10]. ...
Bio-Psycho-Social Therapy for Stress-Induced Chronic Pain Abstract. Against the background of latest neurobiological and epigenetic findings the bio-psycho-social model of disease is outlined often misinterpreted in the context of chronic pain. It represents the basic principle for a personalized treatment of stress-induced chronic pain. Consequences for diagnostic procedures are delineated to detect this pathogenetic subgroup of chronic pain patients (e.g. fibromyalgia, back pain, temporomandibular dysfunction, tension headache). Finally, the principles of a bio-psycho-social treatment program with high efficiency are presented.
... gen zunehmend berücksichtigt. Hingegen werden als weiterer pathogenetischer Mechanismus stressinduzierte Schmerzerkrankungen (9,45,12) in der Diagnostik chronischer Schmerzerkrankungen weiterhin kaum berücksichtigt, bei denen weder ein nozizeptiver noch ein neuropathischer Befund als schmerzverursachend erhoben werden können. Trotzdem leiden die betroffenen Patienten unter Dauerschmerzen, die durch medikamentöse oder invasive Massnahmen nicht hinreichend beeinflussbar sind. ...
... ). Chronischer Stress kann aufgrund eines erhöhten Cortisolspiegels zu toxischen Schädigungen in Amygdala, Hippocampus und vorderem Gyrus cinguli führen, d. h. in jenen Bereichen der zentralen Schmerzverarbeitung, die gleichzeitig auch für die Stressverarbeitung zuständig sind. Akuter Stress unterdrückt kurzfristig das Schmerzempfinden, chronischer Stress verstärkt es(Egle et al. 2016). Die vermehrte Cortisolausschüttung führt zusätzlich zu einer Schwächung der Immunabwehr und zu einer vermehrten Parodontitisaktivität. ...
Bruxism and myoarthrophathy lead to a complex set of burdens that can involve both medical and psychological aspects. Muscular tension due to stress affects these burdens and leads to chronic pain. Using a stress model, it was explained how the individual processing of stress leads to varying negative effects on oral health and jaw function. Through a short survey, it is possible for the dentist to assess the extent of the chronic pain and the associated psychosocial burdens, and, when necessary, encourage the patient to undertake psychological guidance. By learning relaxation techniques and pain coping mechanisms, the pain can be reduced. In order to achieve a long lasting successful treatment, one must consider both medical and psychosomatic aspects.
... Ein pathogenetisches Modell zum klinischen Verständnis funktioneller Schmerzsyndrome stellt das Modell der stressinduzierten Hyperalgesie (SIH) dar. Roth und Egle (2016) undEgle et al. (2016) berichteten, dass biologische und psychosoziale Stressoren in der frühen Entwicklung zu einer erhöhten Schmerzvulnerabilität im späteren Leben führen können, so dass Schmerz sogar ganz ohne peripheren Input (z. B. eine Verletzung) ausschließlich zentral (im Gehirn) generiert wird.Darüber hinaus kann die Theorie der gemeinsamen neuronalen Substrate zur Erklärung von körperlichen Schmerzen und psychischen Leiden nach Eisenberger (2012) einbezogen werden. ...
Viele Menschen mit chronischen Schmerzen berichten über traumatische oder belastende Erfahrungen wie körperliche Misshandlung und sexuellen Missbrauch. In dieser Metaanalyse wurde die Häufigkeit von Misshandlungserfahrungen in der Kindheit bei Erwachsenen mit chronischen Schmerzzuständen untersucht. Zusätzlich wurde das relative Risiko für das Auftreten chronischer Schmerzen unter Personen, die über Misshandlungserfahrungen in der Kindheit berichteten, eingeschätzt. Es wurde eine systematische Literaturrecherche der Beiträge von 2001 bis 2018 und Metaanalysen unter Berücksichtigung von Geschlecht und der Misshandlungsform als Moderatoren
durchgeführt. Identifiziert wurden insgesamt zwölf Studien mit N = 77 533 Personen. Durchschnittlich 30.85 % (95 % CI [21.99 % – 41.39 %]) der Personen mit chronischen Schmerzen berichteten über Misshandlungserfahrungen in der Kindheit, am häufigsten über körperliche Misshandlung. Frauen teilten häufiger Misshandlungserfahrungen als Männer mit. Es lag ein erhöhtes relatives Risiko für chronische Schmerzen unter Personen mit Misshandlungserfahrungen in der Kindheit im Vergleich zu Personen ohne solche Erfahrungen vor (RR = 1.18, 95 % CI [1.14, 1.23]). Die Ergebnisse deuten darauf hin, dass Misshandlungserfahrungen in der Kindheit mit der Entstehung und ufrechterhaltung von chronischen Schmerzen in Zusammenhang stehen können. Unbearbeitete traumatische Erfahrungen sollten daher bei der Diagnostik und Betreuung von Menschen mit chronischen Schmerzen berücksichtigt werden.
... Based on our qualitative initial online survey, however, we assume -as Kolossa (quoted after Sonnenmoser 2010), that the questioned therapists had experienced trauma in their own life, hence felt drawn to work with trauma victims, but that their work with victims triggers their own, still unprocessed stress-processing disorders and are hence reflected in high symptom values. Sufficiently documented, though, are the findings that emotional deprivation and psychological violence during childhood lead to hyperalgesia in adulthood (Egle 2017, Egle, Egloff & Känel 2016, so that physiological predispositions for hyperalgesia in therapists as well as patients are an early propensity. ...
Over the last few years, the limitations of ‚talking cures' have become more and more apparent, particularly in stress-processing disorders. For this reason, myriad therapy techniques that systematically include body experiences and therewith achieve faster improvement of wellbeing have been developed over the last 30 years. One of these new approaches are the TRE tension and trauma releasing exercises: they are based on the natural human reflex of folding up into fetal position in case of danger and threat (fetal response), and the release of this tension through muscle tremor and shaking oneself off once the danger is over.
With our surveys, we show that trauma consequences do not diminish in general the subjective state of health, but in fact very specific body parts and functions, including the knee and feet, heart, stomach, headache, sleep, and fatigue.
To release these stress reactions we provide a Youtube video to demonstrate the 7 simple exercises
https://www.youtube.com/watch?v=UWTBb_qJd7s&feature=emb_logo
... Hyperalgesie aufgrund früherer konfliktträchtiger Stresserfahrungen (vgl. Egle et al., 2016) reduziert werden kann? Ein grundlegendes methodisches Vorgehen der KZPT IKP ist es, zunächst die Erschöpfung oder die Wutausbrüche mit dem Körper in Verbindung zu setzen. ...
Burnout multidimensionality in body-centered psychotherapy
Burnout clearly reflects the two faces of today’s society: the performers, sacrifice, strength, high motivation, and perfectionism – in contrast to fatigue, exhaustion, lethargy, and chronic somatic symptoms like back pain. This article provides a theoretical overview of the most common terminology of burnout and its core components of emotional exhaustion, cynicism, and reduced self-efficacy. Burnout should not only be seen as a causal result of workplace factors, but also from a multifactorial and multidimensional perspective. This is
illustrated by the Anthropological Cube Model, the core concept of the body oriented psychotherapy IKP. This integrative psychotherapy method is based on the Gestalt approach. It is characterized by process and resource orientation, Emotion and focusing on needs, as well as activation of experiences. Burnout is not only due to past experiences, but also to a lack of adaptability and integration in our high-performance-oriented
era. In the sense of a humanistic therapy, the communication in the «here and now» is of the essence. Also important are the integration of physical symptoms, the emphasis on self-responsibility and the strengthening of autonomy and self-realization. Burnout should therefore be regarded as the clinical expression of a combination of the different dimensions shown in the Anthropological cube model IKP body, psyche, social, spirituality, room, and time.
Pain associated with lateral epicondylopathy is often attributed to some form of mechanical overstrain. However, the possibility of spontaneous pain without a causal mechanical background is rarely part of our differential diagnostic considerations. The data do not exclusively support mechanical causality in lateral epicondylopathy. Neurovegetative factors play a crucial role in chronic myofascial disorders and segmental dysfunctions. These relationships must be taken into account. A unilateral focus on local findings fails to adequately address the consequences of central sensitization effects. Current therapeutic approaches need to place greater emphasis on addressing dysfunctions in myofascial chains and vertebrogenic blockages to prevent chronic courses of lateral epicondylopathy.
Vulvodynia occurs in at least 10% of women worldwide bit is usually only recognized years later. The women affected are severely psychologically, physically and sexually impaired.
After exclusion of infections, neurological, dermatological or neoplastic diseases, the diagnostic criteria are pain and burning sensation for at least 3 months spontaneously or when touching/penetration in the entire vulva and anal region or localized at the tip of the clitoris, vestibule, etc. For the anamnesis and diagnostics, calmness, enough time and understanding are required. Bacteriological smears and sample excisions are not necessary (but can provide indications for treatment, e.g., detection of pathological neuroproliferation or numbers of mast cells) but pH measurement, native preparations, fungal culture if necessary and the Q‑tip test for exploration of the pain zone should be performed.
The treatment options include multimodal, interdisciplinary therapy (physiotherapy, pain therapy, behavioral therapy) in cases of failure of inpatient psychosomatic treatment and vestibulectomy as a last resort with well-defined indications.
The diagnosis of myofascial pain syndrome is usually made after structural-morphological explanations have been ruled out. The lack of positive findings to guide treatment inevitably leaves room for interpretation despite the extensive use of all imaging, neurophysiological or serological diagnostics. Under these circumstances, a careful differential diagnosis must be made between functional and structural aspects, both of which in many cases must be assessed in their different relevance. Particular attention must be paid to indications of vegetative-sympathetic adjustment disorders.
The great importance of a clinical, experience-based approach to this symptom pattern becomes clear here, especially if the technical diagnostic data is of no help. The dominance of imaging findings naturally promotes a structure-based, mechanistic understanding of the illness. In contrast, the emotional, vegetative mood of the patient should be given greater consideration as a diagnostic and therapeutic focus. Treatment measures should have a high success rate, as persistent reductions in stimulus thresholds may lead to prognostically unfavorable chronification.
Different types of body-focused psychological interventions are described and research results presented, partly from meta-analysis : Brainspotting (David Grand), Emotional Freedom technique EFT (Gary Craig), music therapy and Tension and Trauma Release Exercises TRE (David Berceli). Further scientific hypothesis are discussed why and how these interventions might work.
Background:
Most patients suffering from chronic pain are more susceptible to pain and pressure due to higher pain sensitivity. Since psychosocial factors play a central role in developing and maintaining chronic pain, investigating associations between pain sensitivity and psychosocial stressors promises to advance the biopsychosocial understanding of chronic pain.
Objectives:
We aimed to replicate Studer et al.'s (2016) findings about associations of psychosocial stressors with pain sensitivity in a new sample of patients with chronic primary pain (ICD-11, MG30.0).
Methods:
A pain provocation test was used on both middle fingers and earlobes to assess pain sensitivity among 460 inpatients with chronic primary pain. Potentially life-threatening accidents, war experiences, relationship problems, certified inability to work, and adverse childhood experiences were assessed as potential psychosocial stressors. Structural equation modeling was used to investigate associations between psychosocial stressors and pain sensitivity.
Results:
We partially replicated Studer et al.'s findings. Similar to the original study, patients with chronic primary pain showed enhanced pain sensitivity values. Within the investigated group, war experiences (β = 0.160, p < .001) and relationship problems (β = 0.096, p = .014) were associated with higher pain sensitivity. In addition, the control variables of age, sex, and pain intensity also showed a predictive value for higher pain sensitivity. Unlike Studer et al., we could not identify a certified inability to work as a predictor of higher pain sensitivity.
Conclusions:
This study showed that beyond age, sex, and pain intensity, the psychosocial stressors of war experiences and relationship problems were associated with higher pain sensitivity.
Introduction
Low back pain (LBP) leads to considerable impairment of quality of life worldwide and is often accompanied by psychosomatic symptoms.
Objectives
First, to assess the association between stress and chronic low back pain (CLBP) and its simultaneous appearance with fatigue and depression as a symptom triad. Second, to identify the most predictive stress-related pattern set for CLBP for a 1-year diagnosis.
Methods
In a 1-year observational study with four measurement points, a total of 140 volunteers (aged 18–45 years with intermittent pain) were recruited. The primary outcomes were pain [characteristic pain intensity (CPI), subjective pain disability (DISS)], fatigue, and depressive mood. Stress was assessed as chronic stress, perceived stress, effort reward imbalance, life events, and physiological markers [allostatic load index (ALI), hair cortisol concentration (HCC)]. Multiple linear regression models and selection procedures for model shrinkage and variable selection (least absolute shrinkage and selection operator) were applied. Prediction accuracy was calculated by root mean squared error (RMSE) and receiver-operating characteristic curves.
Results
There were 110 participants completed the baseline assessments (28.2 ± 7.5 years, 38.1% female), including HCC, and a further of 46 participants agreed to ALI laboratory measurements. Different stress types were associated with LBP, CLBP, fatigue, and depressive mood and its joint occurrence as a symptom triad at baseline; mainly social-related stress types were of relevance. Work-related stress, such as “excessive demands at work”[ b = 0.51 (95%CI -0.23, 1.25), p = 0.18] played a role for upcoming chronic pain disability. “Social overload” [ b = 0.45 (95%CI -0.06, 0.96), p = 0.080] and “over-commitment at work” [ b = 0.28 (95%CI -0.39, 0.95), p = 0.42] were associated with an upcoming depressive mood within 1-year. Finally, seven psychometric (CPI: RMSE = 12.63; DISS: RMSE = 9.81) and five biomarkers (CPI: RMSE = 12.21; DISS: RMSE = 8.94) could be derived as the most predictive pattern set for a 1-year prediction of CLBP. The biomarker set showed an apparent area under the curve of 0.88 for CPI and 0.99 for DISS.
Conclusion
Stress disrupts allostasis and favors the development of chronic pain, fatigue, and depression and the emergence of a “hypocortisolemic symptom triad,” whereby the social-related stressors play a significant role. For translational medicine, a predictive pattern set could be derived which enables to diagnose the individuals at higher risk for the upcoming pain disorders and can be used in practice.
Objective
There is evidence that experiencing childhood trauma and life stressors across the lifespan together with lower resilience is associated with chronic pain-related conditions. The aim of this study was to explore the potential mediating role of resilience in the relationship between childhood trauma and long-term pain and to explore a possible moderating role of serious life stressors in the last year.
Methods
The participants, drawn from a representative sample of citizens of the Czech Republic (n = 1800, mean age: 46.6 years, 48.7% male), were asked to report various long-term pain conditions, childhood trauma (Childhood Trauma Questionnaire, CTQ), life stressors (Life Stressor Checklist Revised, LSC-R) and resilience (Brief Resilience Scale, BRS) in a cross-sectional face-to-face study conducted in 2016. A conditional process SEM model of moderated mediation was performed.
Results
The occurrence of life stress events affecting the participant’s last year moderated the relationship between childhood trauma, resilience and health. In the group of participants who experienced at least one life stress event affecting their last year, resilience fully mediated the effect of past childhood trauma on long-term pain. In participants who did not experience life stressors with an impact on the last year, the direct path from childhood trauma to health through resilience lost its significance.
Conclusion
The subjective meaning of stress events on one’s life has an impact on the trajectory between childhood trauma and health and acts as a moderator. Resilience may buffer the negative effect of trauma on later long-term pain.
Zusammenfassung Vor dem Hintergrund neuer neurobiologischer und epigenetischer Erkenntnisse erfolgt eine genauere Darstellung des (fachlich oft missverstandenen) "bio-psycho-sozialen" Schmerzverständnisses und seine Bedeutung für das Verständnis stressinduzierter Schmerzzustände als Grundlage einer individualisierten ("personenbezogenen") Schmerztherapie. Daraus werden die Konsequenzen für die Diagnostik bei stressbedingten Schmerzzuständen (z.B. Fibromyalgie-Syndrom, nicht-radikuläre Rückenschmerzen, craniomandibuläre Dysfunktion, Spannungskopfschmerz) abgeleitet. Vor diesem Hintergrund werden die Prinzipien eines hoch wirksamen bio-psycho-sozialen Therapiekonzept skizziert.
Abstract Against the background of latest neurobiological and epigenetic findings the bio-psycho-social model of disease is outlined often misinterpreted in the context of chronic pain. It represents the basic principle for a personalized treatment of stress-induced chronic pain. Consequences for diagnostic procedures are delineated to detect this pathogenetic subgroup of chronic pain patients (e.g. fibromyalgia, back pain, temporomandibular dysfunction, tension headache). Finally the principles of a bio-psycho-social treatment program with high efficiency are presented.
In den letzten Jahren wurden zunehmend die Grenzen der „Talking Cures“ deutlich, insbesondere bei Stressverarbeitungsstörungen. Deshalb wurden in den letzten 30 Jahren viele Therapietechniken entwickelt, die die körperlichen Erfahrungen systematisch in den therapeutischen Prozess einbeziehen, um somit schneller und nachhaltiger Verbesserungen im Befinden zu erreichen. Eines dieser neuen Verfahren sind die TRE Tension, Stress and Trauma Releasing Exercises: Sie basieren auf dem natürlichen menschlichen Reflex, sich bei Gefahr und Bedrohung in die Fötus-Position zu begeben („fetal response“) und nach Ende der Gefahr diese Anspannung wieder aufzulösen und durch Muskelzittern abzuschütteln. – Mit unseren Befragungen können wir zeigen, dass diese Traumafolgen nicht unspezifisch den subjektiven Gesundheitszustand beeinträchtigen, sondern sehr spezifisch bestimmte Körperteile und Funktionen in Mitleidenshaft gezogen werden, insbesondere Knie und Füße, Herz, Magen, Kopfschmerzen, Schlaf und Müdigkeit. Die Anwendung der TRE führen zur Verminderung dieser Beschwerden, sowohl bei den befragten TraumatherapeutInnen im deutschsprachigen Raum als auch bei Soldaten im Kriegsgebiet in der Ostukraine. Dieses Youtube-Video zeigt die 7 TRE-Übungen
https://www.youtube.com/watch?v=UWTBb_qJd7s&feature=emb_logo
Die Daten sind konsistent mit den Vorhersagen, die die Polyvagaltheorie von Porges oder die Defense Cascade von Kozlowska und Kollegen machen.
Background: The adverse childhood experience (ACE) study found that risk for depression increased as a function of number of types of childhood maltreatment, and interpret this as a result of cumulative stress. An alternative hypothesis is that risk depends on type and timing of maltreatment. This will also present as a linear increase, since exposure to more types of abuse increases likelihood of experiencing a critical type of abuse at a critical age.
Methods: 560 (223M/337F) young adults (18–25 years) were recruited from the community without regard to diagnosis and balanced to have equal exposure to 0–4 plus types of maltreatment. The Maltreatment and Abuse Chronology of Exposure Scale assessed severity of exposure to 10 types of maltreatment across each year of childhood. Major depressive disorder (MDD) and current symptoms were evaluated by SCID, interview, and self-report. Predictive analytics assessed importance of exposure at each age and evaluated whether exposure at one or two ages was a more important predictor than number, severity, or duration of maltreatment across childhood.
Results: The most important predictors of lifetime history of MDD were non-verbal emotional abuse in males and peer emotional abuse (EA) in females at 14 years of age, and these were more important predictors across models than number of types of maltreatment (males: t9 = 16.39, p < 10⁻⁷; females t9 = 5.78, p < 10⁻⁴). Suicidal ideation was predicted, in part, by NVEA and peer EA at age 14, but most importantly by parental verbal abuse at age 5 in males and sexual abuse at age 18 in females.
Conclusion: This study provides evidence for sensitive exposure periods when maltreatment maximally impacts risk for depression, and provides an alternative interpretation of the ACE study results. These findings fit with emerging neuroimaging evidence for regional sensitivity periods. The presence of sensitive exposure periods has important implications for prevention, preemption, and treatment of MDD.
Arnold 1 · T. Brinkschmidt 2 · H.-R. Casser 3 · A. Diezemann 3 · I. Gralow 4 · D. Irnich 5 · U. Kaiser 6 · B. Klasen 2 · K. Klimczyk 7 · J. Lutz 8 · B. Nagel 3 · M. Pfingsten 9 · R. Sabatowski 6 · R. Schesser 7 · M. Schiltenwolf 10 · D. Seeger 9 · W. Söllner 11 1 Abteilung für Schmerztherapie, Klinikum Dachau, Dachau 2 Algesiologikum, München 3 DRK Schmerz-Zentrum Mainz, Mainz 4 Schmerzambulanz und Schmerz-Tagesklinik, Klinik für Anästhesiologie, operative Intensivmedizin und Schmerztherapie, Universitätsklinikum Münster, Münster 5 Interdisziplinäre Schmerzambulanz, Klinik für Anaesthesiologie, Klinikum der Universität München, München 6 UniversitätsSchmerzCentrum, Universitätsklinikum Carl Gustav Carus, Technische Universität Dresden, Dresden 7 Interdisziplinäres Schmerzzentrum, m&i-Fachklinik Enzensberg, Hopfen am See 8 Interdisziplinäre Schmerztherapie, Zentralklinik Bad Berka, Bad Berka 9 Schmerztagesklinik und -ambulanz, Zentrum für Anaesthesiologie, Rettungs- und Intensivmedizin, Universitätsmedizin Göttingen, Göttingen 10 Bereich konservative Orthopädie, Schmerztherapie, Klinik für Orthopädie und Unfallchirurgie, Universitätsklinikum Heidelberg, Heidelberg 11 Klinik für Psychosomatische Medizin & Psychotherapie und Interdisziplinäre Schmerztagesklinik, Paracelsus Medizinische Privatuniversität, Klinikum Nürnberg, Nürnberg Multimodale Schmerztherapie für die Behandlung chronischer Schmerzsyndrome Ein Konsensuspapier der Ad-hoc-Kommission Multimodale interdisziplinäre Schmerztherapie der Deutschen Schmerzgesellschaft zu den Behandlungsinhalten Einleitung
Chronic pain and posttraumatic stress disorder (PTSD) are disabling conditions that affect biological, psychological and social domains of functioning. Clinical research demonstrates that patients who suffer from chronic pain and PTSD in combination experience greater pain, affective distress, and disability than patients with either condition alone. Additional research is needed to delineate the interrelated pathophysiology of chronic pain and PTSD, with the goal of facilitating more effective therapies to treat both conditions more effectively; current treatment strategies for chronic pain associated with PTSD have limited efficacy and place a heavy burden on patients, who must visit various specialists in order to manage these conditions separately. This article focuses on neurobiological factors that may contribute to the co-prevalence and synergistic interactions of chronic pain and PTSD. First we outline how circuits that mediate emotional distress and physiological threat, including pain, converge. Secondly, we discuss specific neurobiological mediators and modulators of these circuits that may contribute to chronic pain and PTSD symptoms. For example, neuropeptide Y (NPY), and the neuroactive steroids allopregnanolone and pregnanolone (together termed ALLO) have anti-stress and anti-nociceptive properties. Reduced levels of NPY and ALLO have been implicated in the pathophysiology of both chronic pain and PTSD. The potential contribution of opioid and cannabinoid system factors also will be discussed. Finally, we address potential novel methods to restore the normal function of these systems. Such novel perspectives regarding disease and disease management are vital to the pursuit of relief for the many individuals who struggle with these disabling conditions.
Obwohl die Posttraumatische Belastungsstörung (PTBS) aufgrund ihrer Häufigkeit zu den wichtigen Diifferentialdiagnosen bei chronischen Schmerzzuständen gehört, wird sie oft lange übersehen. Dies gilt auch für die sozialmedizinische Begutachtung. Diese wird zusätzlich noch dadurch erschwert, dass im ICD-10 und im DSM-IV verschiedene Definitionen des Krankheitsbildes bestehen. Das neue DSM-5 hat noch eine weitere Definition hinzugefügt. Die vorliegende Übersicht gibt eine Orientierung für eine valide Diagnostik. Diese bildet die Grundlage für eine differenzierte Begutachtung in den verschiedenen Rechtsgebieten (u.a. Strafrecht, gesetzliche bzw. private Unfallversicherung, Rentenversicherung), bei denen seitens des Gutachters unterschiedliche Anforderungen zu berücksichtigen sind. Ausführlich wird auch auf die Erkennung von Simulation bei der PTBS-Begutachtung eingegangen, die in allen Rechtsgebieten eine zunehmend größere Rolle spielt.
Posttraumatic Stress Disorder (PTSD) is one of the most relevant disorders of patients with chronic pain, but often underdiagnosed. That applies to expert testimony too. An additional difficulty are the different definitions of PTSD in ICD-10 and DSM-IV; the new DSM-5 adds an other one. The present review aims to give a guidance for making valid diagnosis. That forms the basis for a sophisticated expert testimony. In the different fields of law the expert has to meet different requirements. At length the recognition of malingering is described, playing a major role in PTSD-expert testimony in all fields of law.
Pain in infancy influences pain reactivity in later life, but how and why this occurs is poorly understood. Here we review the evidence for developmental plasticity of nociceptive pathways in animal models and discuss the peripheral and central mechanisms that underlie this plasticity. Adults who have experienced neonatal injury display increased pain and injury-induced hyperalgesia in the affected region but mild injury can also induce widespread baseline hyposensitivity across the rest of the body surface, suggesting the involvement of several underlying mechanisms, depending upon the type of early life experience. Peripheral nerve sprouting and dorsal horn central sensitization, disinhibition and neuroimmune priming are discussed in relation to the increased pain and hyperalgesia, while altered descending pain control systems driven, in part, by changes in the stress/HPA axis are discussed in relation to the widespread hypoalgesia. Finally, it is proposed that the endocannabinoid system deserves further attention in the search for mechanisms underlying injury-induced changes in pain processing in infants and children.
To explore patterns of experienced stress and stress reactions before the onset of illness in the life history of patients with severe somatoform disorders to identify predisposing stress-mechanisms.
A systematic, thematic analysis was conducted on data collected from 24 semi-structured individual life history interviews.
Generally, patients had experienced high psychosocial stress during childhood/youth. However, there was considerable variability. Characteristic of all patients were narrations of how communication with significant adults about problems, concerns, and emotions related to stress were experienced to be difficult. The patients described how this involved conflicts stemming from perceived absent, insufficient, or dismissive communication during interactions with significant adults. We conceptualized this empirically based core theme as "emotional avoidance culture." Further, three related subthemes were identified: Generally, patients 1.) experienced difficulties communicating problems, concerns, and related complex feelings in close social relations; 2.) adapted their emotional reactions and communication to an emotional avoidance culture, suppressing their needs, vulnerability and feelings of sadness and anger that were not recognized by significant adults; and 3.) disconnected their stress reaction awareness from stressful bodily sensations by using avoidant behaviors e.g. by being highly active.
Patients adapted to an emotional avoidance culture characterized by difficult and conflicting communication of concerns and related emotions in social interactions with significant adults. Patients experienced low ability to identify and express stress-related cognitions, emotions and feelings, and low bodily and emotional self-contact, which made them vulnerable to stressors. Generally, patients resolved stress by avoidant behaviors, prolonging their stress experience.
Up to 80% of patients with severe posttraumatic stress disorder are suffering from “unexplained” chronic pain. Theories about the links between traumatization and chronic pain have become the subject of increased interest over the last several years. We will give a short summary about the existing interaction models that emphasize particularly psychological and behavioral aspects of this interaction. After a synopsis of the most important psychoneurobiological mechanisms of pain in the context of traumatization, we introduce the hypermnesia–hyperarousal model, which focuses on two psychoneurobiological aspects of the physiology of learning. This hypothesis provides an answer to the hitherto open question about the origin of pain persistence and pain sensitization following a traumatic event and also provides a straightforward explanatory model for educational purposes.
Einleitung
Daten zur administrativen Prävalenz, Behandlung und zu den Krankheitskosten der somatoformen Schmerzstörung (ICD-10 F45.4x) aus Deutschland lagen bisher nicht vor.
Material und Methoden
Die Abrechnungsdaten von 8,5 Mio. Versicherten der BARMER GEK wurden für den Zeitraum von 2008 bis 2010 ausgewertet. Analysiert wurden die Alters- und Geschlechtsprävalenz, Anteile der Fachrichtungen an der Versorgung, die durchgeführte Diagnostik und Therapie und Krankheitskosten bei Versicherten mit mindestens einer F45.4x-Codierung in 2009 sowie mindestens einer weiteren F45.4x-Codierung im Zeitraum von 2008 bis 2010. Die Abrechnungsdaten der kassenärztlichen Vereinigung für die ambulante Behandlung und die der Krankenhäuser für die stationäre Behandlung wurden ausgewertet.
Ergebnisse
Die administrative Prävalenz verdoppelte sich von 2008 bis 2010 nach der Aufteilung des F45.4 in F45.40 und F45.41. Die Diagnose F45.4x wurde 2009 bei 0,5 % der Versicherten gestellt, bei Frauen 2,3-mal häufiger als bei Männern. Hausärzte (41 %) und Anästhesisten (28 %) bildeten die hauptversorgenden Gruppen. Im Jahr 2009 wurden 54 % der Patienten einer Röntgenaufnahme unterzogen, 25 % einer Magnetresonanztomographie und 11 % einer Computertomographie. Leistungen der psychosomatischen Grundversorgung erhielten 66 % der Patienten, 38 % Verordnungen eines Opioids, 12 % Spinalnervenanalgesie und 14 % ambulante Psychotherapie. Die durchschnittlichen jährlichen direkten und indirekten Krankheitskosten pro Patient mit somatoformer Schmerzstörung lagen 2009 bei 5500 €.
Schlussfolgerung
Versicherte mit somatoformer Schmerzstörung wurden möglicherweise mit bildgebenden und invasiven Verfahren sowie mit Opioiden über- und fehlversorgt.
Fibromyalgia (FM) is a clinically well-defined chronic condition of unknown aetiology characterized by chronic widespread pain that often co-exists with sleep disturbances, cognitive dysfunction and fatigue. Patients often report high disability levels and negative mood. Psychotherapies focus on reducing key symptoms, improving daily functioning, mood and sense of personal control over pain.
To assess the benefits and harms of cognitive behavioural therapies (CBTs) for treating FM at end of treatment and at long-term (at least six months) follow-up.
We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2013, Issue 8), MEDLINE (1966 to 28 August 2013), PsycINFO (1966 to 28 August 2013) and SCOPUS (1980 to 28 August 2013). We searched http://www.clinicaltrials.gov (web site of the US National Institutes of Health) and the World Health Organization Clinical Trials Registry Platform (ICTRP) (http://www.who.int/ictrp/en/) for ongoing trials (last search 28 August,2013), and the reference lists of reviewed articles.
We selected randomised controlled trials of CBTs with children, adolescents and adults diagnosed with FM.
The data of all included studies were extracted and the risks of bias of the studies were assessed independently by two review authors. Discrepancies were resolved by discussion.
Twenty-three studies with 24 study arms with CBTs were included. A total of 2031 patients were included; 1073 patients in CBT groups and 958 patients in control groups. Only two studies were without any risk of bias. The GRADE quality of evidence of the studies was low. CBTs were superior to controls in reducing pain at end of treatment by 0.5 points on a scale of 0 to 10 (standardised mean difference (SMD) - 0.29; 95% confidence interval (CI) -0.49 to -0.17) and by 0.6 points at long-term follow-up (median 6 months) (SMD -0.40; 95% CI -0.62 to -0.17); in reducing negative mood at end of treatment by 0.7 points on a scale of 0 to 10 (SMD - 0.33; 95% CI -0.49 to -0.17) and by 1.3 points at long-term follow-up (median 6 months) (SMD -0.43; 95% CI -0.75 to -0.11); and in reducing disability at end of treatment by 0.7 points on a scale of 0 to 10 (SMD - 0.30; 95% CI -0.51 to -0.08) and at long-term follow-up (median 6 months) by 1.2 points (SMD -0.52; 95% CI -0.86 to -0.18). There was no statistically significant difference in dropout rates for any reasons between CBTs and controls (risk ratio (RR) 0.94; 95% CI 0.65 to 1.35).
CBTs provided a small incremental benefit over control interventions in reducing pain, negative mood and disability at the end of treatment and at long-term follow-up. The dropout rates due to any reason did not differ between CBTs and controls.
Objective:
Childhood maltreatment increases risk for psychopathology. For some highly prevalent disorders (major depression, substance abuse, anxiety disorders, and posttraumatic stress disorder) a substantial subset of individuals have a history of maltreatment and a substantial subset do not. The authors examined the evidence to assess whether those with a history of maltreatment represent a clinically and biologically distinct subtype.
Method:
The authors reviewed the literature on maltreatment as a risk factor for these disorders and on the clinical differences between individuals with and without a history of maltreatment who share the same diagnoses. Neurobiological findings in maltreated individuals were reviewed and compared with findings reported for these disorders.
Results:
Maltreated individuals with depressive, anxiety, and substance use disorders have an earlier age at onset, greater symptom severity, more comorbidity, a greater risk for suicide, and poorer treatment response than nonmaltreated individuals with the same diagnoses. Imaging findings associated with these disorders, such as reduced hippocampal volume and amygdala hyperreactivity, are more consistently observed in maltreated individuals and may represent a maltreatment-related risk factor. Maltreated individuals also differ from others as a result of epigenetic modifications and genetic polymorphisms that interact with experience to increase risk for psychopathology.
Conclusions:
Phenotypic expression of psychopathology may be strongly influenced by exposure to maltreatment, leading to a constellation of ecophenotypes. While these ecophenotypes fit within conventional diagnostic boundaries, they likely represent distinct subtypes. Recognition of this distinction may be essential in determining the biological bases of these disorders. Treatment guidelines and algorithms may be enhanced if maltreated and nonmaltreated individuals with the same diagnostic labels are differentiated.
Experimental stress has been shown to have analgesic as well as allodynic effect in animals. Despite the obvious negative influence of stress in clinical pain conditions, stress-induced alteration of pain sensitivity has not been tested in humans so far. Therefore, we tested changes of pain sensitivity using an experimental stressor in ten female healthy subjects and 13 female patients with fibromyalgia.
Multiple sensory aspects of pain were evaluated in all participants with the help of the quantitative sensory testing protocol before (60 min) and after (10 and 90 min) inducing psychological stress with a standardized psychosocial stress test ("Trier Social Stress Test").
Both healthy subjects and patients with fibromyalgia showed stress-induced enhancement of pain sensitivity in response to thermal stimuli. However, only patients showed increased sensitivity in response to pressure pain.
Our results provide evidence for stress-induced allodynia/hyperalgesia in humans for the first time and suggest differential underlying mechanisms determining response to stressors in healthy subjects and patients suffering from chronic pain. Possible mechanisms of the interplay of stress and mediating factors (e.g. cytokines, cortisol) on pain sensitivity are mentioned. Future studies should help understand better how stress impacts on chronic pain conditions.
A review of the literature was conducted to assess the association between oxytocin (OT) and pain.
PsychInfo, PubMed, and Medline (EBSCO) research databases were searched for peer-reviewed articles written between 1950 and 2012. Of a total of 1166 articles returned, 50 (9 human, 33 animal, and 8 spinal cord samples) met full inclusion criteria and were included in the review.
OT had a reliable effect as defined by increasing pain tolerance in 29 of 33 animal studies reviewed. This effect persisted across central and peripheral modes of administration and type of noxious stimulus used (eg, heat, electric). The results suggest that OT acts as an analgesic for acute pain in animals. Preliminary research with humans offers consistent evidence to suggest that OT decreases pain sensitivity, though the reliability and stability of such effects cannot yet be determined. Although the findings are encouraging, there is a need for methodologically rigorous work in humans where OT is administered centrally.
Further research seems to be warranted as the existence of biologically and psychologically plausible mechanisms linking OT and pain have been well supported using animal models with limited but encouraging human research. Implications and recommendations are discussed. Findings from this research may inform therapeutic methods for the management of pain.
In der Betreuung von chronischen Schmerzpatienten greifen Erklärungsmodelle, welche auf der Nachweisbarkeit von peripheren organischen Befunden beharren oder – bei deren Nichtnachweisbarkeit – direkt auf eine Psychologisierung der Schmerzen umschwenken, oftmals zu kurz. Der heutige Wissensstand verlangt nach einer differenzierteren Betrachtungsweise, welche neurobiologische und neuropsychische Aspekte des Schmerzerlebens integriert
Chronic pain is one of the most prevalent health problems in our modern world, with millions of people debilitated by conditions such as back pain, headache and arthritis. To address this growing problem, many people are turning to mind-body therapies, including meditation, yoga and cognitive behavioural therapy. This article will review the neural mechanisms underlying the modulation of pain by cognitive and emotional states - important components of mind-body therapies. It will also examine the accumulating evidence that chronic pain itself alters brain circuitry, including that involved in endogenous pain control, suggesting that controlling pain becomes increasingly difficult as pain becomes chronic.
Background:
Early-life stress and exposure to stressful stimuli play a major role in the development of chronic widespread pain in adults. However, how they interact in chronic pain syndromes remains unclear.
Methods:
Dams and neonatal litters were submitted to a restriction of nesting material (neonatal limited bedding [NLB]) for 1 week. As adults, these rats were exposed to a painless sound stress protocol. The involvement of sympathoadrenal catecholamines interleukin 6 (IL-6) and tumor necrosis factor alpha (TNFα) in nociception was evaluated through behavioral and enzyme-linked immunosorbent assays, surgical interventions, and intrathecal antisense treatments.
Results:
Adult NLB rats exhibited mild muscle hyperalgesia, which was markedly aggravated by sound stress (peaking 15 days after exposure). Adrenal medullectomy did not modify hyperalgesia in NLB rats but prevented its aggravation by sound stress. Sustained administration of epinephrine to NLB rats mimicked sound stress effect. Intrathecal treatment with antisense directed to IL-6 receptor subunit gp130 (gp130), but not to tumor necrosis factor receptor type 1 (TNFR1), inhibited hyperalgesia in NLB rats. However, antisense against either gp130 or TNFR1 inhibited sound stress-induced enhancement of hyperalgesia. Compared with control rats, NLB rats exhibit increased plasma levels of IL-6 but decreased levels of TNFα, whereas sound stress increases IL-6 plasma levels in control rats but not in NLB rats.
Conclusions:
Early-life stress induces a persistent elevation of IL-6, hyperalgesia, and susceptibility to chronic muscle pain, which is unveiled by exposure to stress in adults. This probably depends on an interaction between adrenal catecholamines and proinflammatory cytokines acting at muscle nociceptor level.
Background
Current diagnostic systems for mental disorders rely upon presenting signs and symptoms, with the result that current definitions do not adequately reflect relevant neurobiological and behavioral systems - impeding not only research on etiology and pathophysiology but also the development of new treatments.
Discussion
The National Institute of Mental Health began the Research Domain Criteria (RDoC) project in 2009 to develop a research classification system for mental disorders based upon dimensions of neurobiology and observable behavior. RDoC supports research to explicate fundamental biobehavioral dimensions that cut across current heterogeneous disorder categories. We summarize the rationale, status and long-term goals of RDoC, outline challenges in developing a research classification system (such as construct validity and a suitable process for updating the framework) and discuss seven distinct differences in conception and emphasis from current psychiatric nosologies.
Summary
Future diagnostic systems cannot reflect ongoing advances in genetics, neuroscience and cognitive science until a literature organized around these disciplines is available to inform the revision efforts. The goal of the RDoC project is to provide a framework for research to transform the approach to the nosology of mental disorders.
Predictions about sensory input exert a dominant effect on what we perceive, and this is particularly true for the experience of pain. However, it remains unclear what component of prediction, from an information-theoretic perspective, controls this effect. We used a vicarious pain observation paradigm to study how the underlying statistics of predictive information modulate experience. Subjects observed judgments that a group of people made to a painful thermal stimulus, before receiving the same stimulus themselves. We show that the mean observed rating exerted a strong assimilative effect on subjective pain. In addition, we show that observed uncertainty had a specific and potent hyperalgesic effect. Using computational functional magnetic resonance imaging, we found that this effect correlated with activity in the periaqueductal gray. Our results provide evidence for a novel form of cognitive hyperalgesia relating to perceptual uncertainty, induced here by vicarious observation, with control mediated by the brainstem pain modulatory system.
CHRONIC FATIGUE SYNDROME (CFS) and the related fibromyalgia (FM) syndrome are largely overlapping disorders, mainly characterized by long-lasting, medically unexplained physical and mental fatigue, effort intolerance and widespread musculoskeletal pain. Consensus diagnostic criteria have been formulated for both syndromes (Fukuda et al., 1994; Wolfe et al., 1990), but the definition and delineation of the syndromes remain controversial (Nimnuan et al., 2001; Reeves et al., 2003; Wessely and White, 2004), and even the very existence of the syndromes has been a matter of debate (Van Houdenhove, 2003). Despite intensive research efforts, many questions with regard to the etiological determinants and pathogenetic mechanisms of the syndromes remain unresolved. Nonetheless, evidence is growing that chronic physical and/or psychosocial stress may play a predisposing, precipitating, and perpetuating role in CFS as well as in FM (Prins et al., 2006; Van Houdenhove and Egle, 2004). Evidently, stress may take different forms, such as negative life events (e.g., death of a spouse, divorce), daily hassles (e.g., persistent job problems, family conflicts), or the burden of an overactive lifestyle (e.g., due to excessive perfectionism, or self-sacrificing care-giving). But besides these 2 common stresses in adulthood, many clinicians have been struck by the high prevalence of early life stress and particularly early traumatic or victimization experiences (i.e., maltreatment, abuse, and/or neglect) in the history of CFS and FM patients (Van Houdenhove et al., 2001a). During the past decades, the prevalence and long-term consequences of early life stress have been intensively studied, and it is now believed that such experiences may play an etio-pathogenetic role in many psychiatric and physical disorders in later life (Arnow, 2004; Egle et al., 2005; Kendall-Tackett, 2004; McCauley et al., 1995, 1997). However, systematic investigations on the possible link between early life stress and chronic pain or fatigue have not led to unequivocal conclusions. Hence, some authors plead for more investigations in this domain (Kendall-Tackett, 2001), but others warn of multiple methodological pitfalls threatening this endeavour (Raphael et al., 2004; Raphael, 2005). In this chapter, we will examine the evidence for these connections through summaries of both controlled studies on childhood trauma in FM and CFS patients, and two of our own studies in a mixed CFS/FM sample. These results help us consider the multiple and complex pathways that may lead from victimization to chronic pain and fatigue as well as methodological problems inherent of research on this topic. These issues and their implications for practice are discussed in light of both an illustrative case report and suggested connections between research findings in clinical terms, and we propose some guidelines for health care providers.
Although pediatric functional abdominal pain (FAP) has been linked to abdominal pain later in life, childhood predictors of long-term outcomes have not been identified. This study evaluated whether distinct FAP profiles based on patterns of pain and adaptation in childhood could be identified and whether these profiles predicted differences in clinical outcomes and central sensitization (wind-up) on average 9years later. In 843 pediatric FAP patients, cluster analysis was used to identify subgroups at initial FAP evaluation based on profiles of pain severity, gastrointestinal (GI) and non-GI symptoms, pain threat appraisal, pain coping efficacy, catastrophizing, negative affect, and activity impairment. Three profiles were identified: high pain dysfunctional, high pain adaptive, and low pain adaptive. Logistic regression analyses controlling for age and sex showed that, compared with pediatric patients with the low pain adaptive profile, those with the high pain dysfunctional profile were significantly more likely at long-term follow-up to meet criteria for pain-related functional gastrointestinal disorder (FGID) (odds ratio: 3.45, confidence interval: 1.95 to 6.11), FGID with comorbid nonabdominal chronic pain (odds ratio: 2.6, confidence interval: 1.45 to 4.66), and FGID with comorbid anxiety or depressive psychiatric disorder (odds ratio: 2.84, confidence interval: 1.35 to 6.00). Pediatric patients with the high pain adaptive profile had baseline pain severity comparable to that of the high pain dysfunctional profile, but had outcomes as favorable as the low pain adaptive profile. In laboratory pain testing at follow-up, high pain dysfunctional patients showed significantly greater thermal wind-up than low pain adaptive patients, suggesting that a subgroup of FAP patients has outcomes consistent with widespread effects of heightened central sensitization.
Human neuroimaging offers a powerful way to connect animal and human research on emotion, with profound implications for psychological science. However, the gulf between animal and human studies remains a formidable obstacle: human studies typically focus on the cortex and a few subcortical regions such as the amygdala, whereas deeper structures such as the brainstem periaqueductal gray (PAG) play a key role in animal models. Here, we directly assessed the role of PAG in human affect by interleaving in a single fMRI session two conditions known to elicit strong emotional responses-physical pain and negative image viewing. Negative affect and PAG activity increased in both conditions. We next examined eight independent data sets, half featuring pain stimulation and half negative image viewing. In sum, these data sets comprised 198 additional participants. We found increased activity in PAG in all eight studies. Taken together, these findings suggest PAG is a key component of human affective responses.
It is well established that psychosocial work stressors relate to employees' work-related musculoskeletal disorder (WRMSD) symptoms. Using a model investigating psychological strain as a mediator between work stressors and WRMSD complaints, this study demonstrated that high levels role conflict, low job control, and low safety-specific leadership are associated with increased employee strain. Strain, in turn, was related to higher levels of WRMSD symptoms of the wrist/hand, shoulders, and lower back. Partial mediation of some relationships was also found, suggesting that additional meditational mechanisms for the relationships between stressors and musculoskeletal symptoms are plausible. This work supports the notion that psychosocial stressors in the work environment have important links to employee health, especially WRMSDs.
Although it has long been hypothesized that attachment figures provide individuals with a sense of safety and security, the neural mechanisms underlying attachment-induced safety have not been explored. Here, we investigated whether an attachment figure acts as a safety signal by exploring whether viewing an attachment figure during a threatening experience (physical pain) led to increased activity in a neural region associated with safety signaling, the ventromedial prefrontal cortex (VMPFC), and corresponding reductions in pain. Female participants in long-term romantic relationships were scanned as they received painful stimuli while viewing pictures of their partner and control images (stranger, object). Consistent with the idea that the attachment figure may signal safety, results revealed that viewing partner pictures while receiving painful stimulation led to reductions in self-reported pain ratings, reductions in pain-related neural activity (dorsal anterior cingulate cortex, anterior insula), and increased activity in the VMPFC. Moreover, greater VMPFC activity in response to partner pictures was associated with longer relationship lengths and greater perceived partner support, further highlighting a role for the VMPFC in responding to the safety value of the partner. Last, greater VMPFC activity while viewing partner pictures was associated with reduced pain ratings and reduced pain-related neural activity. An implication of these findings is that, in the same way that stimuli that historically have threatened survival (e.g., snakes, spiders) are considered to be prepared fear stimuli, attachment figures, who have historically benefited survival, may serve as prepared safety stimuli, reducing threat- or distress-related responding in their presence.
The aim of this study was to examine whether familial risk factors for the development of somatoform symptoms and somatoform disorders in children and adolescents can be deduced from studies which investigated the intergenerational transmission of functional abdominal pain and somatoform disorders. A systematic review of articles published in English and German since 1990 was performed. Twenty-three relevant studies were found. The following putative familial risk factors for the development of somatoform symptoms and somatoform disorders were identified: somatization of parents, organic disease of a significant other, psychopathology of close family members, dysfunctional family climate, traumatic experiences in childhood and insecure attachment. Most of the putative familial risk factors are associated with many other psychiatric child disorders and are therefore mostly nonspecific. Further longitudinal studies, in which comorbidity and other putative risk factors are taken into account, are needed to identify specific familial risk factors for the development of somatoform symptoms and somatoform disorders.
Fragestellung: In der vorliegenden Arbeit wird der Zusammenhang zwischen den Coping-Strategien von Patienten mit somatoformen Storungen und Leitsymptom Schmerz einerseits und Kindheitsbelastungsfaktoren andererseits untersucht. Berucksichtigt wird das Vorhandensein einer psychischen Komorbiditat. Methode: 327 konsekutiv untersuchte Patienten erfullten die Kriterien einer somatoformen Schmerzstorung oder einer Somatisierungsstorung mit Leitsymptom Schmerz. Bei allen Patienten wurde sowohl eine SKID-I- und SKID-II-Diagnostik als auch eine strukt. biograph. Anamnese (MSBA) durchgefuhrt. Die Coping-Strategien wurden mithilfe des Coping Strategy Questionnaires (CSQ), dt. Version, erfasst. Ergebnisse: Hoheres „Katastrophisieren“ ist mit der psychischen Erkrankung eines Elternteils, emotionaler Vernachlassigung und haufigem Streit zwischen den Eltern assoziiert. Katastrophisieren ist zudem in der Gruppe der Patienten mit komorbiden psychischen Erkrankungen erhoht, die Gruppe, die mehr Kindheitsbelastungsfaktoren aufweist. Bei vorhandenem sexuellem Missbrauch ist lediglich das Schmerzverhalten verstarkt, wahrend bei korperlicher Misshandlung in der Kindheit die Coping-Strategien „Umdeuten“ und „Selbstinstruktion“ in hoherem Mase eingesetzt werden. In der Stichprobe zeigt sich daruber hinaus kein eindeutiger Zusammenhang zwischen der Kumulation von Kindheitsbelastungsfaktoren und eingesetzten Coping-Strategien. Diskussion: Die Ergebnisse zeigen, dass innerhalb einer symptomhomogenen Patientengruppe Unterschiede hinsichtlich der Coping-Strategien bestehen. Diese sind nur teilweise auf eine unterschiedliche Kumulation von Kindheitsbelastungsfaktoren in den Subgruppen zuruckzufuhren. Vielmehr zeigten reale Beziehungserfahrungen in der Kindheit einen Zusammenhang mit der Bevorzugung bestimmter Coping-Strategien im Erwachsenenalter.
The locus coeruleus noradrenergic (LC-NE) system is one of the first systems engaged following a stressful event. While numerous groups have demonstrated that LC-NE neurons are activated by many different stressors, the underlying neural circuitry and the role of this activity in generating stress-induced anxiety has not been elucidated. Using a combination of in vivo chemogenetics, optogenetics, and retrograde tracing, we determine that increased tonic activity of the LC-NE system is necessary and sufficient for stress-induced anxiety and aversion. Selective inhibition of LC-NE neurons during stress prevents subsequent anxiety-like behavior. Exogenously increasing tonic, but not phasic, activity of LC-NE neurons is alone sufficient for anxiety-like and aversive behavior. Furthermore, endogenous corticotropin-releasing hormone(+) (CRH(+)) LC inputs from the amygdala increase tonic LC activity, inducing anxiety-like behaviors. These studies position the LC-NE system as a critical mediator of acute stress-induced anxiety and offer a potential intervention for preventing stress-related affective disorders.
Copyright © 2015 Elsevier Inc. All rights reserved.
Objective
This meta-analysis systematically examined the association of reported psychological trauma and posttraumatic stress disorder (PTSD) with functional somatic syndromes including fibromyalgia, chronic widespread pain, chronic fatigue syndrome, temporomandibular disorder, and irritable bowel syndrome. Our goals were to determine the overall effect size of the association and to examine moderators of the relationship.Methods
Literature searches identified 71 studies with a control or comparison group and examined the association of the syndromes with traumatic events including abuse of a psychological, emotional, sexual, or physical nature sustained during childhood or adulthood, combat exposure, or PTSD. A random-effects model was used to estimate the pooled odds ratio and 95% confidence interval. Planned subgroup analyses and meta-regression examined potential moderators.ResultsIndividuals who reported exposure to trauma were 2.7 (95% confidence interval = 2.27-3.10) times more likely to have a functional somatic syndrome. This association was robust against both publication bias and the generally low quality of the literature. The magnitude of the association with PTSD was significantly larger than that with sexual or physical abuse. Chronic fatigue syndrome had a larger association with reported trauma than did either irritable bowel syndrome or fibromyalgia. Studies using nonvalidated questionnaires or self-report of trauma reported larger associations than did those using validated questionnaires.Conclusions
Findings highlight the limitations of the existing literature and emphasize the importance of conducting prospective studies, further examining the potential similarities and differences of these conditions and pursuing hypothesis-driven studies of the mechanisms underlying the link between trauma, PTSD, and functional somatic syndromes.
Unlabelled:
Case-control studies have consistently associated psychological factors with chronic pain in general and with temporomandibular disorder (TMD) specifically. However, only a handful of prospective studies have explored whether preexisting psychological characteristics represent risk factors for first-onset TMD. The current findings derive from the prospective cohort study of the Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) cooperative agreement. For this study, 3,263 TMD-free participants completed a battery of psychological instruments assessing general psychological adjustment and personality, affective distress, psychosocial stress, somatic symptoms, and pain coping and catastrophizing. Study participants were then followed prospectively for an average of 2.8 years to ascertain cases of first-onset of TMD, and 2,737 provided follow-up data and were considered in the analyses of TMD onset. In bivariate and demographically adjusted analyses, several psychological variables predicted increased risk of first-onset TMD, including reported somatic symptoms, psychosocial stress, and affective distress. Principal component analysis of 26 psychological scores was used to identify latent constructs, revealing 4 components: stress and negative affectivity, global psychological and somatic symptoms, passive pain coping, and active pain coping. In multivariable analyses, global psychological and somatic symptoms emerged as the most robust risk factor for incident TMD. These findings provide evidence that measures of psychological functioning can predict first onset of TMD. Future analyses in the OPPERA cohort will determine whether these psychological factors interact with other variables to increase risk for TMD onset and persistence.
Perspective:
This article reports that several premorbid psychological variables predict first-onset TMD in the OPPERA study, a large prospective cohort study designed to discover causal determinants of TMD pain. Measures of somatic symptoms were most strongly associated with TMD onset, but perceived stress, previous life events, and negative affect also predicted TMD incidence.
Cross-sectional studies have shown that chronic musculoskeletal pain and somatic symptoms are frequently reported by sexual assault (SA) survivors; however, prospective studies examining pain and somatic symptoms in the months after SA have not been performed.
Women SA survivors 18 years of age or older who presented for care within 48 h of SA were recruited. Pain in eight body regions (head and face, neck, breast, arms, abdomen, back, genital and pelvic, and legs) and 21 common somatic symptoms (e.g., headache, nausea, insomnia, persistent fatigue) were assessed (0-10 numeric rating scale in each body region) at the time of presentation, 1-week, 6-week and 3-month interview. Post-traumatic stress disorder (PTSD) symptoms were assessed at the 6-week and 3-month interview.
Clinically significant new or worsening pain (CSNWP) symptoms were common among study participants 6 weeks after SA [43/74, 58% (95% CI, 47-69%)] and 3 months after SA [40/67, 60% (95% CI, 48-71%)] and generally occurred in regions not experiencing trauma. Women SA survivors also experienced an increased burden of many common somatic symptoms: 8/21 (38%) and 11/21 (52%) common somatic symptoms showed a significant increase in severity 6 weeks and 3 months after SA, respectively. Correlations between PTSD, CSNWP and somatic symptoms were only low to moderate, suggesting that these outcomes are distinct.
New and/or clinically worsening pain and somatic symptoms, lasting at least 3 months, are sequelae of SA. Further studies investigating pain and somatic symptoms after SA are needed.
Objective
There is vast evidence to support the presence of brain aberrations in patients with fibromyalgia (FM), and it is possible that central plasticity is critical for the transition from acute to chronic pain. The aim of the present study was to investigate the relationship between brain structure and function in patients with FM. Methods
Functional connectivity of the brain during application of intermittent pressure-pain stimuli and measures of brain structure were compared between 26 patients with FM and 13 age- and sex-matched healthy controls. Magnetic resonance imaging (MRI) was performed to obtain high-resolution anatomic images and functional MRI scans of the brain, which were used for measurements of pain-evoked brain activity. ResultsFM patients displayed a distinct overlap between decreased cortical thickness, decreased brain volumes, and decreased functional regional coherence in the rostral anterior cingulate cortex. The morphometric changes were more pronounced with longer exposure to FM pain. In addition, there was evidence of an association between structural and functional changes in the mesolimbic areas of the brain and the severity of comorbid depression symptoms in FM patients. Conclusion
The combined integration of structural and functional measures allowed for a unique characterization of the impact of FM pain on the brain. These data may lead to the identification of early structural and functional brain alterations in response to pain, which could be used to develop markers for predicting the development of FM and other pain disorders.
The general principles formulated in this paper may be summarized as follows: 1.1. What is experienced and reported as pain is a psychological phenomenon. Pain does not come into being without the operation of the psychic mechanisms which give rise to its indentifiable qualities and which permit its perception. In neurophysiological terms this also means there is no pain without the participation of higher nervous centers.2.2. Developmentally, however, pain evolves from patterns of impulses arising from peripheral receptors which are part of the basic biologic nocioceptive system for the protection of the organism from injury. The psychic experience, pain, develops phylogenetically and ontogenetically from what was originally only a reflex organization. This may be compared to the necessity for functioning eyes and ears to receive light and sound waves before the complex psychic experiences of seeing and hearing can evolve.3.3. Once the psychic organization necessary for pain has evolved, the experience, pain, no longer requires peripheral stimulation to be provoked, just as visual and auditory sensations (hallucinations) may occur without sense organ input. When such are projected outside the mind (in contrast to a painful thought or a painful frame of mind) they are felt as being in some part of the body and are to the patient indistinguishable from pain arising in the periphery.4.4. Since the experience, pain, and the sensory experiences from which it evolves are part of the biologic equipment whereby the individual learns about the environment and about his body, and since this has a special function as a warning or indicator of damage to body parts, pain plays an important role in the total psychologic development of the individual. Indeed, pain, along with other affects, comes to occupy a key position in the regulation of the total psychic economy. We discover that in the course of the child's development, pain and relief of pain enter into the formation of interpersonal (object) relations and into the concepts of good and bad, reward and punishment, success and failure. Pain becomes par excellence a means of assuaging guilt and thereby influences object relationships.5.5. From the clinical viewpoint we discover that disordered neural patterns originating in the periphery confer certain qualities on the pain experience that permit the physician to recognize their presence and hence make a presumptive diagnosis of an organic lesion.6.6. Clinical psychological studies of all varieties of patients with pain reveal that some individuals are more prone than others to use pain as a psychic regulator, whether the pain includes a peripheral source of stimulation or not. These pain-prone individuals usually show some or all of the following features: 6.1.(1) A prominance of conscious and unconscious guilt, with pain serving as a relatively satisfactory means of atonement.6.2.(2) A background that tends to predispose to the use of pain for such purposes.6.3.(3) A history of suffering and defeat and intolerance of success (masochistic character structure). A propensity to solicit pain, as evidenced by the large number of painful injuries, operations and treatments.6.4.(4) A strong aggressive drive which is not fulfilled, pain being experienced instead.6.5.(5) Development of pain as a replacement for a loss at times when a relationship is threatened or lost.6.6.(6) A tendency toward a sado-masochistic type of sexual development, with some episodes of pain occurring in settings of conflict over sexual impulses.6.7.(7) A location of pain determined by unconscious identification with a love object, the pain being either one suffered by the patient himself when in some conflict with the object or a pain suffered by the object in fact or in the patient's fantasy.6.8.(8) Psychiatric diagnoses include conversion hysteria, depression, hypochondriasis and paranoid schizophrenia, or mixtures of these. Some patients with pain do not fit into any distinct nosologie category.
It is now well established that pain is a multidimensional phenomenon, affected by a gamut of psychosocial and biological variables. According to diathesis–stress models of chronic pain, some individuals are more vulnerable to developing disability following acute pain because they possess particular psychosocial vulnerabilities which interact with physical pathology to impact negatively upon outcome. Attachment theory, a theory of social and personality development, has been proposed as a comprehensive developmental model of pain, implicating individual adult attachment pattern in the ontogenesis and maintenance of chronic pain. The present paper reviews and critically appraises studies which link adult attachment theory with chronic pain. Together, these papers offer support for the role of insecure attachment as a diathesis (or vulnerability) for problematic adjustment to pain. The Attachment-Diathesis Model of Chronic Pain developed from this body of literature, combines adult attachment theory with the diathesis–stress approach to chronic pain. The evidence presented in this review, and the associated model, advances our understanding of the developmental origins of chronic pain conditions, with potential application in guiding early pain intervention and prevention efforts, as well as tailoring interventions to suit specific patient needs.
Objectives:
There is evidence that education on pain physiology can have positive effects on pain, disability, and catastrophization in patients with chronic musculoskeletal pain disorders. A double-blind randomized controlled trial (RCT) was performed to examine whether intensive pain physiology education is also effective in fibromyalgia (FM) patients, and whether it is able to influence the impaired endogenous pain inhibition of these patients.
Methods:
Thirty FM patients were randomly allocated to either the experimental (receiving pain physiology education) or the control group (receiving pacing self-management education). The primary outcome was the efficacy of the pain inhibitory mechanisms, which was evaluated by spatially accumulating thermal nociceptive stimuli. Secondary outcome measures included pressure pain threshold measurements and questionnaires assessing pain cognitions, behavior, and health status. Assessments were performed at baseline, 2 weeks, and 3 months follow-up. Repeated measures ANOVAS were used to reveal possible therapy effects and effect sizes were calculated.
Results:
After the intervention the experimental group had improved knowledge of pain neurophysiology (P<0.001). Patients from this group worried less about their pain in the short term (P=0.004). Long-term improvements in physical functioning (P=0.046), vitality (P=0.047), mental health (P<0.001), and general health perceptions (P<0.001) were observed. In addition, the intervention group reported lower pain scores and showed improved endogenous pain inhibition (P=0.041) compared with the control group.
Discussion:
These results suggest that FM patients are able to understand and remember the complex material about pain physiology. Pain physiology education seems to be a useful component in the treatment of FM patients as it improves health status and endogenous pain inhibition in the long term.
The purpose of this study was to examine the associations between dimensions of perfectionism (self-oriented, other-oriented, and socially prescribed perfectionism) and health functioning in a sample of 489 women with fibromyalgia.
Hierarchical multiple regression was used to determine whether dimensions of perfectionism were differentially associated with health functioning among women with fibromyalgia after accounting for broader personality traits related to both perfectionism and health functioning.
The results confirmed that both socially prescribed perfectionism and self-oriented perfectionism were associated with lower health functioning. Moreover, these associations were found after accounting for the effects of conscientiousness, extraversion, and neuroticism. The findings involving self-oriented perfectionism were particularly complex and suggested that moderate self-oriented perfectionism may be somewhat adaptive, but too much or too little self-oriented perfectionism is associated with substantial reductions in health functioning among women with fibromyalgia.
Collectively, these findings clarify that overall levels of perfectionism are not elevated among women with fibromyalgia, but those women who are exceptionally high in levels of self-oriented perfectionism or high in socially prescribed perfectionism are particularly likely to suffer lower health functioning. These results suggest that perfectionism should be specifically assessed and targeted for intervention among women with fibromyalgia and there should be a particular emphasis on the pressure to meet perceived or actual expectations imposed on the self.
Experiences of social rejection, exclusion or loss are generally considered to be some of the most 'painful' experiences that we endure. Indeed, many of us go to great lengths to avoid situations that may engender these experiences (such as public speaking). Why is it that these negative social experiences have such a profound effect on our emotional well-being? Emerging evidence suggests that experiences of social pain--the painful feelings associated with social disconnection--rely on some of the same neurobiological substrates that underlie experiences of physical pain. Understanding the ways in which physical and social pain overlap may provide new insights into the surprising relationship between these two types of experiences.
For over 30 years, scientists have been investigating the phenomenon of pain suppression upon exposure to unconditioned or conditioned stressful stimuli, commonly known as stress-induced analgesia. These studies have revealed that individual sensitivity to stress-induced analgesia can vary greatly and that this sensitivity is coupled to many different phenotypes including the degree of opioid sensitivity and startle response. Furthermore, stress-induced analgesia is influenced by age, gender, and prior experience to stressful, painful, or other environmental stimuli. Stress-induced analgesia is mediated by activation of the descending inhibitory pain pathway. Pharmacological and neurochemical studies have demonstrated involvement of a large number of neurotransmitters and neuropeptides. In particular, there are key roles for the endogenous opioid, monoamine, cannabinoid, γ-aminobutyric acid and glutamate systems. The study of stress-induced analgesia has enhanced our understanding of the fundamental physiology of pain and stress and can be a useful approach for uncovering new therapeutic targets for the treatment of pain and stress-related disorders.
The neural circuitry of fear likely underlies anxiety and fear-related disorders such as specific and social phobia, panic disorder, and posttraumatic stress disorder. The primary pharmacological treatments currently utilized for these disorders include benzodiazepines, which act on the GABAergic receptor system, and antidepressants, which modulate the monamine systems. However, recent work on the regulation of fear neural circuitry suggests that specific neuropeptide modulation of this system is of critical importance. Recent reviews have examined the roles of the hypothalamic-pituitary-adrenal axis neuropeptides as well as the roles of neurotrophic factors in regulating fear. The present review, instead, will focus on three neuropeptide systems which have received less attention in recent years but which are clearly involved in regulating fear and its extinction. The endogenous opioid system, particularly activating the μ opioid receptors, has been demonstrated to regulate fear expression and extinction, possibly through functioning as an error signal within the ventrolateral periaqueductal gray to mark unreinforced conditioned stimuli. The cholecystokinin (CCK) system initially led to much excitement through its potential role in panic disorder. More recent work in the CCK neuropeptide pathway suggests that it may act in concordance with the endogenous cannabinoid system in the modulation of fear inhibition and extinction. Finally, older as well as very recent data suggests that neuropeptide Y (NPY) may play a very interesting role in counteracting stress effects, enhancing extinction, and enhancing resilience in fear and stress preclinical models. Future work in understanding the mechanisms of neuropeptide functioning, particularly within well-known behavioral circuits, are likely to provide fascinating new clues into the understanding of fear behavior as well as suggesting novel therapeutics for treating disorders of anxiety and fear dysregulation.
The aim of the study was to determine the prevalence of psychiatric disorders in patients referred to a tertiary pain clinic. The temporal relationship between the onset of pain and depression and anxiety and the association of psychiatric disorders with pain intensity were also analyzed.
One hundred consecutive outpatients underwent a psychiatric assessment using the Structured Clinical Interview and Statistical Manual of Mental Disorders Axis I.
The psychiatric disorders diagnosed for the past 12 months included major depressive (37%), anxiety (25%) and substance use disorder (12%). The prevalence of any lifetime psychiatric disorder was 75%. Most anxiety disorders (77%) had been present before pain onset, whereas 63% of the depressive disorders appeared after the onset of pain. Psychiatric morbidity was associated with increased pain intensity.
Chronic pain patients have a remarkable psychiatric morbidity. A structured diagnostic interview, covering a large range of psychiatric diagnoses, allows a more comprehensive approach to the assessment of the patient. This should improve the management of chronic pain. However, prospective studies are needed to show this.
Chronic pain in adults has been associated with early-life stress. To examine the pronociceptive effect of early-life stress, we evaluated cutaneous and muscle nociception and activity in muscle nociceptors in an animal model of neonatal stress, limited bedding, in the rat. In this neonatal limited bedding (NLB) model, litters are exposed to limited bedding between postnatal days 2 and 9, and controls to standard bedding. In adult NLB-treated rats, mechanical nociceptive threshold in skeletal muscle was significantly lower (~22%) than in controls. Furthermore, administration of prostaglandin E(2) in skin as well as muscle produced markedly prolonged hyperalgesia, an effect prevented by spinal intrathecal injection of oligodeoxynucleotide antisense to protein kinase Cε (PKCε), a second messenger in nociceptors that has been implicated in the induction and maintenance of chronic pain. In electrophysiological studies, mechanical threshold of muscle nociceptors was reduced by ~31% and conduction velocity significantly increased (~28%). These findings indicate that neonatal stress induces a persistent hyperalgesia and nociceptor sensitization manifest in the adult and that the second messenger PKCε may be a target against which therapies might be directed to treat a chronic pain syndrome that is associated with early-life traumatic stress.
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'.