ORCID Profile
0000-0003-0437-6665
Current Organisation
Maastricht University
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Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 2019
DOI: 10.1097/J.PAIN.0000000000001365
Abstract: The upcoming 11th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD) of the World Health Organization (WHO) offers a unique opportunity to improve the representation of painful disorders. For this purpose, the International Association for the Study of Pain (IASP) has convened an interdisciplinary task force of pain specialists. Here, we present the case for a reclassification of nervous system lesions or diseases associated with persistent or recurrent pain for ≥3 months. The new classification lists the most common conditions of peripheral neuropathic pain: trigeminal neuralgia, peripheral nerve injury, painful polyneuropathy, postherpetic neuralgia, and painful radiculopathy. Conditions of central neuropathic pain include pain caused by spinal cord or brain injury, poststroke pain, and pain associated with multiple sclerosis. Diseases not explicitly mentioned in the classification are captured in residual categories of ICD-11 . Conditions of chronic neuropathic pain are either insufficiently defined or missing in the current version of the ICD, despite their prevalence and clinical importance. We provide the short definitions of diagnostic entities for which we submitted more detailed content models to the WHO. Definitions and content models were established in collaboration with the Classification Committee of the IASP's Neuropathic Pain Special Interest Group (NeuPSIG). Up to 10% of the general population experience neuropathic pain. The majority of these patients do not receive satisfactory relief with existing treatments. A precise classification of chronic neuropathic pain in ICD-11 is necessary to document this public health need and the therapeutic challenges related to chronic neuropathic pain.
Publisher: Oxford University Press (OUP)
Date: 28-09-2016
DOI: 10.1093/PM/PNW221
Abstract: Associative learning has been proposed as a mechanism behind the persistence of pain after tissue healing. The simultaneous occurrence of nociceptive and non-nociceptive input during acute injury mimics the pairings thought to drive classical conditioning effects. However, empirical evidence for classically conditioned allodynia is lacking. We aimed to manipulate pain thresholds with a classical conditioning procedure that used non-nociceptive somatosensory stimuli as conditioned stimuli (CS) and nociceptive stimuli as unconditioned stimuli. We also explored the influence of gender, depression, anxiety, negative affect, and pain catastrophizing on the main manipulation. Thirty-four healthy humans participated in a differential classical conditioning procedure that used vibrotactile stimulations at two different locations as CS. In an acquisition phase, CS+ was paired with painful thermal stimulation, and CS- with nonpainful thermal stimulation. Heat pain threshold was assessed during paired heat-CS trials before and after acquisition. A 2 (time: 1 and 2) x 2 (condition: CS+ and CS-) repeated-measures analysis of variance compared pain thresholds before and after acquisition. Exploratory analyses explored the influence of gender, depression, anxiety, negative affect, and pain catastrophizing. Postexperiment questions investigated participants' awareness of the contingencies employed. The classical conditioning procedure did not alter pain thresholds. Exploratory analyses did not reveal any influence of in idual differences. Thirty of the 34 participants were unaware of the contingencies between stimuli. The results of this study provide no evidence that allodynia can be induced in healthy humans using a classical conditioning procedure with simultaneous timing.
Publisher: PeerJ
Date: 08-03-2019
DOI: 10.7717/PEERJ.6486
Abstract: Classical conditioning has frequently been shown to be capable of evoking fear of pain and avoidance behavior in the context of chronic pain. However, whether pain itself can be conditioned has rarely been investigated and remains a matter of debate. Therefore, the present study investigated whether pain threshold ratings can be modified by the presence of conditioned non-nociceptive sensory stimuli in healthy participant. In 51 healthy volunteers, pain threshold to electrocutaneous stimuli was determined prior to participation in a simultaneous conditioning paradigm. Participants underwent an acquisition phase in which one non-painful vibrotactile stimulus (CS + ) was repeatedly paired with a painful electrocutaneous stimulus, whereas a second vibrotactile stimulus of the same quality and intensity (CS − ) was paired with a non-painful electrocutaneous stimulus. Stimulation was provided on the lower back with close proximity between the conditioned stimulus and the unconditioned stimulus. In the test phase, electrocutaneous stimuli at the in idually-set threshold intensity were simultaneously delivered together with either a CS + or CS − . Pain intensity ratings were obtained after each trial expectancy ratings were obtained after each block. The primary outcome was the percentage of test stimuli that were rated as painful. Test stimuli were more likely to be rated as painful when they were paired with the CS + than when they were paired with the CS − . This effect was not influenced by contingency awareness, nor by expectancies or mood states. The findings support the notion that the judgement of an event being painful or non-painful can be influenced by classical conditioning and corroborate the possible role of associative learning in the development and maintenance of chronic pain.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 2015
Publisher: Oxford University Press (OUP)
Date: 14-12-2016
DOI: 10.1093/PM/PNV044
Abstract: Clinical scenarios of repeated pain usually involve both nociceptive and non-nociceptive input. It is likely that associations between these stimuli are learned over time. Such learning may underlie subsequent lification of pain, or evocation of pain in the absence of nociception. We undertook a systematic review and meta-analysis to evaluate the evidence that allodynia or hyperalgesia can be a classically conditioned response. A sensitive search of the literature covered Medline, Embase, CINAHL, AMED, PubMed, Scopus, PsycArticles, PsycINFO, Cochrane Library, and Web of Science. Additional studies were identified by contacting experts and searching published reviews. Two reviewers independently assessed studies for inclusion, evaluated risk of bias, and extracted data. Studies were included if they aimed to elicit or lify pain using a classical conditioning procedure in healthy, adult humans. Studies were excluded if they did not distinguish between classical conditioning and explicit verbal suggestion as learning sources, or did not use experiential learning. Thirteen studies, with varying risk of bias, were included. Ten studies evaluated classically conditioned hyperalgesia: nine found hyperalgesia one did not. Pooled effects (n = 8 with full data) showed a significant pain increase after conditioning (mean difference of 7.40 [95%CI: 4.00-10.80] on a 0-100 pain scale). Three studies evaluated conditioned allodynia and found conflicting results. The existing literature suggests that classical conditioning can lify pain. No conclusions can be drawn about whether or not classical conditioning can elicit pain. Rigorous experimental conditioning studies with nociceptive unconditioned stimuli are needed to fill this gap in knowledge.
Publisher: Elsevier BV
Date: 12-2019
Publisher: Elsevier BV
Date: 10-2016
DOI: 10.1016/J.JPAIN.2016.06.012
Abstract: A classical conditioning framework is often used for clinical reasoning about pain that persists after tissue healing. However, experimental studies demonstrating classically conditioned pain in humans are lacking. The current study tested whether non-nociceptive somatosensory stimuli can come to modulate pain thresholds after being paired with painful nociceptive stimuli in healthy humans. We used a differential simultaneous conditioning paradigm in which one nonpainful vibrotactile conditioned stimulus (CS(+)) was simultaneously paired with an unconditioned painful laser stimulus, and another vibrotactile stimulus (CS(-)) was paired with a nonpainful laser stimulus. After acquisition, at-pain-threshold laser stimuli were delivered simultaneously with a CS(+) or CS(-) vibrotactile stimulus. The primary outcome was the percentage of at-threshold laser stimuli that were reported as painful. The results were as expected: after conditioning, at-threshold laser trials paired with the CS(+) were reported as painful more often, as more intense, and as more unpleasant than those paired with the CS(-). This study provides new evidence that pain thresholds can be modulated via classical conditioning, even when the stimulus used to test the threshold cannot be anticipated. As such, it lays a critical foundation for further investigations of classical conditioning as a possible driver of persistent pain. This study provides new evidence that human pain thresholds can be influenced by non-nociceptive somatosensory stimuli, via a classical conditioning effect. As such, it lays a critical foundation for further investigations of classical conditioning as a possible driver of persistent pain.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 07-2004
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 05-2008
Publisher: Wiley
Date: 30-07-2019
DOI: 10.1111/PSYP.13447
Abstract: Slow, deep breathing is being used as a self-management intervention for various health conditions including pain and hypertension. Stimulation of the arterial baroreceptors and increased vagal modulation are among the proposed mechanisms for the therapeutic effects of slow, deep breathing. We investigated whether adding inspiratory threshold load can enhance the cardiovascular responses to controlled breathing at the frequency of 0.1 Hz, a common form of slow, deep breathing. Healthy volunteers (N = 29) performed controlled breathing at 0.1 Hz (6 breaths/minute) without load and with inspiratory threshold loads of 5 cmH
Publisher: Wiley
Date: 27-10-2021
DOI: 10.1111/PSYP.13712
Publisher: Elsevier BV
Date: 09-2015
DOI: 10.1016/J.BETH.2015.02.004
Abstract: Recent research suggests that the mere intention to perform a painful movement can elicit pain-related fear. Based on these findings, the present study aimed to determine whether imagining a movement that is associated with pain (CS+) can start to elicit conditioned pain-related fear as well and whether pain-related fear elicited by imagining a painful movement can spread towards novel, similar but distinct imagined movements. We proposed a new experimental paradigm that integrates the left-right hand judgment task (HJT) with a differential fear conditioning procedure. During Acquisition, one hand posture (CS+) was consistently followed by a painful electrocutaneous stimulus (pain-US) and another hand posture (CS-) was not. Participants were instructed to make left-right judgments, which involve mentally rotating their own hand to match the displayed hand postures (i.e., motor imagery). During Generalization, participants were presented with a series of novel hand postures with six grades of perceptual similarity to the CS+ (generalization stimuli GSs). Finally, during Extinction, the CS+ hand posture was no longer reinforced. The results showed that (1) a painful hand posture triggers fear and increased US-expectancy as compared to a nonpainful hand posture, (2) this pain-related fear spreads to similar but distinct hand postures following a generalization gradient, and subsequently, (3) it can be successfully reduced during extinction. These effects were apparent in the verbal ratings, but not in the startle measures. Because of the lack of effect in the startle measures, we cannot draw firm conclusions about whether the "imagined movements" (i.e., motor imagery of the hand postures) gained associative strength rather than the hand posture pictures itself. From a clinical perspective, basic research into generalization of pain-related fear triggered by covert CSs such as intentions, imagined movements and movement-related cognitions might further our understanding of how pain and fear avoidance spread and persevere.
Publisher: PeerJ
Date: 20-06-2022
DOI: 10.7717/PEERJ.13512
Abstract: Pain is thought to be influenced by the threat value of the particular context in which it occurs. However, the mechanisms by which a threat achieves this influence on pain are unclear. Here, we explore how threat influences experimentally-induced secondary hyperalgesia, which is thought to be a manifestation of central sensitization. We developed an experimental study to investigate the effect of a manipulation of threat on experimentally-induced secondary hyperalgesia in 26 healthy human adults (16 identifying as female 10 as male). We induced secondary hyperalgesia at both forearms using high-frequency electrical stimulation. Prior to the induction, we used a previously successful method to manipulate threat of tissue damage at one forearm (threat site). The effect of the threat manipulation was determined by comparing participant-rated anxiety, perceived threat, and pain during the experimental induction of secondary hyperalgesia, between the threat and control sites. We hypothesized that the threat site would show greater secondary hyperalgesia (primary outcome) and greater surface area (secondary outcome) of induced secondary hyperalgesia than the control site. Despite a thorough piloting procedure to test the threat manipulation, our data showed no main effect of site on pain, anxiety, or threat ratings during high-frequency electrical stimulation. In the light of no difference in threat between sites, the primary and secondary hypotheses cannot be tested. We discuss reasons why we were unable to replicate the efficacy of this established threat manipulation in our s le, including: (1) competition between threats, (2) generalization of learned threat value, (3) safety cues, (4) trust, and requirements for participant safety, (5) s ling bias, (6) s le-specific habituation to threat, and (7) implausibility of (sham) skin examination and report. Better strategies to manipulate threat are required for further research on the mechanisms by which threat influences pain.
Publisher: Elsevier BV
Date: 05-2020
DOI: 10.1016/J.JPAIN.2019.10.002
Abstract: The aim of the study reported in this paper is to investigate the effect of slow-deep breathing (SDB) on self-reported pain, heart rate variability, and baroreflex sensitivity (BRS). These effects are examined in 3 separate experiments, each using a different phasic pain modality. For each experiment, different subjects were recruited. Eighty-three healthy female participants were instructed to breathe guided by a visual cue at a slow frequency (SDB: .1 Hz), and at a frequency close to the spontaneous breathing frequency (normal paced breathing, .2 Hz). Pain was induced during instructed breathing using electrocutaneous (experiment 1, n = 31), thermal (experiment 2, n = 28), or mechanical stimuli (experiment 3, n = 24). Participants were requested to rate the intensity of each painful stimulus (Numerical Rating Scale) and subjective level of pleasantness, arousal, and dominance (self-assessment manikin). During the experiment, R-R interval, blood pressure, tidal volume, and end-tidal CO
Publisher: Wiley
Date: 11-08-2022
DOI: 10.1111/NMO.14242
Abstract: Studies using somatic pain models have shown the hypoalgesic effects of slow, deep breathing. We evaluated the effect of slow, deep breathing on visceral pain and explored putative mediating mechanisms including autonomic and emotional responses. Fifty‐seven healthy volunteers (36 females, mean age = 22.0 years) performed controlled, deep breathing at a slow frequency (6 breaths per minute), controlled breathing at a normal frequency (14 breaths per minute active control), and uncontrolled breathing (no‐treatment control) in randomized order. Moderate painful stimuli were given during each condition by delivering electrical stimulation in the distal esophagus. Participants rated pain intensity after each stimulation. Heart rate variability and self‐reported arousal were measured during each condition. Compared to uncontrolled breathing, pain intensity was lower during slow, deep breathing (Cohen’s d = 0.40) and normal controlled breathing ( d = 0.47), but not different between slow, deep breathing and normal controlled breathing. Arousal was lower ( d = 0.53, 0.55) and heart rate variability was higher ( d = 0.70, 0.86) during slow, deep breathing compared to the two control conditions. The effect of slow, deep breathing on pain was not mediated by alterations in heart rate variability or arousal but was moderated by pain catastrophizing. Slow, deep breathing can reduce visceral pain intensity. However, the effect is not specific to the slow breathing frequency and is not mediated by autonomic or emotional responses, suggesting other underlying mechanisms (notably distraction). Whether a long‐term practice of slow, deep breathing can influence (clinical) visceral pain warrants to be investigated.
Publisher: Elsevier BV
Date: 10-2017
DOI: 10.1016/J.JPAIN.2017.04.011
Abstract: A growing body of research has identified fear of visceral sensations as a potential mechanism in the development and maintenance of visceral pain disorders. However, the extent to which such learned fear affects visceroception remains unclear. To address this question, we used a differential fear conditioning paradigm with nonpainful esophageal balloon distensions of 2 different intensities as conditioning stimuli (CSs). The experiment comprised of preacquisition, acquisition, and postacquisition phases during which participants categorized the CSs with respect to their intensity. The CS+ was always followed by a painful electrical stimulus (unconditioned stimulus) during the acquisition phase and in 60% of the trials during postacquisition. The second stimulus (CS-) was never associated with pain. Analyses of galvanic skin and startle eyeblink responses as physiological markers of successful conditioning showed increased fear responses to the CS+ compared with the CS-, but only in the group with the low-intensity stimulus as CS+. Computational modeling of response times and response accuracies revealed that differential fear learning affected perceptual decision-making about the intensities of visceral sensations such that sensations were more likely to be categorized as more intense. These results suggest that associative learning might indeed contribute to visceral hypersensitivity in functional gastrointestinal disorders. This study shows that associative fear learning biases intensity judgements of visceral sensations toward perceiving such sensations as more intense. Learning-induced alterations in visceroception might therefore contribute to the development or maintenance of visceral pain.
Publisher: Elsevier BV
Date: 09-2020
DOI: 10.1016/J.JPAIN.2019.12.010
Abstract: Slow deep breathing (SDB) is commonly employed in the management of pain, but the underlying mechanisms remain equivocal. This study sought to investigate effects of instructed breathing patterns on experimental heat pain and to explore possible mechanisms of action. In a within-subject experimental design, healthy volunteers (n = 48) performed 4 breathing patterns: 1) unpaced breathing, 2) paced breathing (PB) at the participant's spontaneous breathing frequency, 3) SDB at 6 breaths per minute with a high inspiration/expiration ratio (SDB-H), and 4) SDB at 6 breaths per minute with a low inspiration/expiration ratio (SDB-L). During presentation of each breathing pattern, participants received painful heat stimuli of 3 different temperatures and rated each stimulus on pain intensity. Respiration, heart rate, and blood pressure were recorded. Compared to unpaced breathing, participants reported less intense pain during each of the 3 instructed breathing patterns. Among the instructed breathing patterns, pain did not differ between PB and SDB-H, and SDB-L attenuated pain more than the PB and SDB-H patterns. The latter effect was paralleled by greater blood pressure variability and baroreflex effectiveness index during SDB-L. Cardiovascular changes did not mediate the observed effects of breathing patterns on pain. PERSPECTIVES: SDB is more efficacious to attenuate pain when breathing is paced at a slow rhythm with an expiration that is long relative to inspiration, but the underlying mechanisms remain to be elucidated.
Publisher: Wiley
Date: 06-07-2021
DOI: 10.1111/PSYP.13895
Abstract: Slow, deep breathing (SDB) is a common pain self‐management technique. Stimulation of the arterial baroreceptors and vagal modulation are suggested, among others, as potential mechanisms underlying the hypoalgesic effects of SDB. We tested whether adding an inspiratory load to SDB, which results in a stronger baroreceptor stimulation and vagal modulation, enhances its hypoalgesic effects. Healthy volunteers performed SDB (controlled at 0.1 Hz) with and without an inspiratory threshold load. Controlled breathing (CB) at a normal frequency (0.23 Hz) was used as an active control. Each condition lasted 90 s, included an electrical pain stimulation on the hand, and was repeated four times in a randomized order. Pain intensity, self‐reported emotional responses (arousal, valence, dominance), and cardiovascular parameters (including vagally‐mediated heart rate variability) were measured per trial. A cover story was used to limit the potential effect of outcome expectancy. Pain intensity was slightly lower during SDB with load compared with normal‐frequency CB, but the effect was negligible (Cohens d 0.2), and there was no other difference in pain intensity between the conditions. Heart rate variability was higher during SDB with/without load compared with normal‐frequency CB. Using load during SDB was associated with higher heart rate variability, but less favorable emotional responses. These findings do not support the role of baroreceptor stimulation or vagal modulation in the hypoalgesic effects of SDB. Other mechanisms, such as attentional modulation, warrant further investigation.
Publisher: Elsevier BV
Date: 10-2014
DOI: 10.1016/J.JPAIN.2014.07.005
Abstract: Contingency learning, in particular the formation of danger beliefs, underpins conditioned fear and avoidance behavior, yet equally important is the formation of safety beliefs. That is, when threat beliefs and accompanying fear/avoidance spread to technically safe cues, it might cause disability. Indeed, such over generalization has been advanced as a trans-diagnostic pathologic marker, but it has not been investigated in chronic pain. Using a novel hand pain scenario contingency learning task, we tested the hypotheses that chronic hand pain patients demonstrate less differential pain expectancy judgments because of poor safety learning and demonstrate broader generalization gradients than healthy controls. Participants viewed digitized 3-dimensional hands in different postures presented in random order (conditioned stimulus [CS]) and rated the likelihood that a fictive patient would feel pain when moving the hand into that posture. Subsequently, the outcome (pain/no pain) was presented on the screen. One hand posture was followed by pain (CS+), another was not (CS-). Generalization was tested using novel hand postures (generalization stimuli) that varied in how similar they were to the original conditioned stimuli. Patients, but not healthy controls, demonstrated a contingency learning deficit determined by impaired safety learning, but not by exaggerated pain expectancy toward the CS+. Patients showed flatter, asymmetric generalization gradients than the healthy controls did, with higher pain expectancy for novel postures that were more similar to the original CS-. The results clearly uphold our hypotheses and suggest that contingency learning deficits might be important in the development and maintenance of the chronic pain-related disability. Chronic hand pain patients demonstrate 1) reduced differential contingency learning determined by a lack of safety belief formation, but not by exaggerated threat belief formation, and 2) flatter, asymmetric generalization gradients than the healthy controls.
Publisher: SAGE Publications
Date: 05-2005
DOI: 10.1191/0269215505CR814OA
Abstract: Objective: To develop a self-report measure for assessment of the stage of change in patients with osteoarthritis, in order to identify patients who would benefit from a self-management programme. Methods: According to the ‘stages of change’ model a questionnaire was developed with three groups of items corresponding to the precontemplation stage (Pre), the contemplation (Cont) and the action (Act) stage. Internal consistency and factor structure of this questionnaire were investigated by assessing Cronbach's alphas and by performing factor analysis. Subjects and setting: The questionnaire was offered to 273 patients who entered a randomized clinical trial on self-management in a general health care setting. Results: Factor analysis revealed that most items corresponded to the a priori described groups, while some items were not loading on the presumed factor. In each subgroup some items were deleted, resulting in a 15-item questionnaire. After this item reduction Cronbach's alphas were 0.72 (Pre), 0.76 (Cont) and 0.79 (Act) and all factor loadings were satisfactory (above 0.35). Classification revealed some differences between parts of the total group, for ex le in the proportion of patients in the preparation stage (recruited by general practitioner 33.6% advertisement 49.2%). Conclusions: The Stages of Change Questionnaire in Osteoarthritis, a 15-item questionnaire to assess the ‘stage of change’ of a patient with osteoarthritis showed good internal consistency and adequate factor structure. These findings warrant further studies on validity and applicability in a clinical context.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 2019
DOI: 10.1097/J.PAIN.0000000000001384
Abstract: Chronic pain is a major source of suffering. It interferes with daily functioning and often is accompanied by distress. Yet, in the International Classification of Diseases , chronic pain diagnoses are not represented systematically. The lack of appropriate codes renders accurate epidemiological investigations difficult and impedes health policy decisions regarding chronic pain such as adequate financing of access to multimodal pain management. In cooperation with the WHO, an IASP Working Group has developed a classification system that is applicable in a wide range of contexts, including pain medicine, primary care, and low-resource environments. Chronic pain is defined as pain that persists or recurs for more than 3 months. In chronic pain syndromes, pain can be the sole or a leading complaint and requires special treatment and care. In conditions such as fibromyalgia or nonspecific low-back pain, chronic pain may be conceived as a disease in its own right in our proposal, we call this subgroup “chronic primary pain.” In 6 other subgroups, pain is secondary to an underlying disease: chronic cancer-related pain, chronic neuropathic pain, chronic secondary visceral pain, chronic posttraumatic and postsurgical pain, chronic secondary headache and orofacial pain, and chronic secondary musculoskeletal pain. These conditions are summarized as “chronic secondary pain” where pain may at least initially be conceived as a symptom. Implementation of these codes in the upcoming 11th edition of International Classification of Diseases will lead to improved classification and diagnostic coding, thereby advancing the recognition of chronic pain as a health condition in its own right.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 10-2015
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 06-2015
No related grants have been discovered for Johannes Vlaeyen.