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Background: Cognitive-affective factors influence the perception of pain and disability. These factors can lead to pain behaviors (PB) that can persist and become maladaptive. These maladaptive PB will further increase the risk of chronicity or persistence of symptoms and disability. Thus, clinicians must be prepared to recognize maladaptive PB in a clinical context. To date, in the context of assessment in a rehabilitation setting, PB in clinical settings are poorly documented. The main objective of this study was to identify direct observation methods and critically appraise them in order to propose recommendations for practice. As a secondary objective, we explored and extracted the different observable PB that patients could exhibit and that clinicians could observe. Methods: We conducted a comprehensive review on four databases with a generic search strategy in order to obtain the largest range of PB. For the first objective, a two-step critical appraisal used clinical criteria (from qualitative studies on barriers to implement routine measures) and psychometric criteria (from Brink and Louw critical appraisal tool) to determine which observation methods could be recommended for clinical practice. For the second objective, we extracted PB found in the literature to list potential PB that patients could exhibit, and clinicians could observe. Results: From the 3362 retrieved studies, 47 met the inclusion criteria for the first objective. The clinical criteria allowed us to select three observation methods. After the psychometric step, two observation methods were retained and recommended for clinical practice: the Behavioral Avoidance Test-Back Pain (BAT-Back) and the Pain Behaviour Scale (PaBS). For the second objective, 107 studies met the inclusion criteria. The extraction of the PB allowed us to list a large range of PB and classify the data in 7 categories of PB. Conclusion: Our results allowed us to recommend two observation methods for clinical practice. H

Serotonin (5-hydroxytryptamine, 5-HT) released by platelets, mast cells, and immunocytes is a potent inflammatory mediator which modulates pain and itch sensing in the peripheral nervous system. The serotonergic receptors expressed by primary afferent neurons involved in these sensory functions are not fully identified and appear to be to a large extent species dependent. Moreover, the mechanisms through which 5-HT receptor activation is coupled to changes in neuronal excitability have not been completely revealed. Using a combination of in vitro (calcium and voltage imaging and patch-clamp) and in vivo behavioral methods, we used both male and female Wistar rats to provide evidence for the involvement of two 5-HT receptor subtypes, 5-HT1A and 5-HT3, in mediating the sustained and transient effects, respectively, of 5-HT on rat primary afferent neurons involved in pain and itch processing. In addition, our results are consistent with a model in which sustained serotonergic responses triggered via the 5-HT1A receptor are due to closure of background potassium channels, followed by membrane depolarization and action potentials, during which the activation of voltage-gated calcium channels leads to calcium entry. Our results may provide a better understanding of mammalian serotonergic itch signaling.

We studied the psychometric properties of the 39-item v1.1 Dutch-Flemish Patient-Reported Outcomes Measurement Information System Pain Behavior item bank in a sample of 1,602 patients with musculoskeletal complaints. We evaluated the assumptions of the underlying item response theory (IRT) model (unidimensionality and local dependency with confirmatory factor analyses), and monotonicity with scalability coefficients). We studied the IRT model fit of all items and estimated the item parameters of the IRT model. Differential item functioning (DIF) was studied for age and gender, and DIF for language was studied as a measure of cross-cultural validity. Confirmatory factor analyses showed suboptimal fit of a unidimensional model, but a bifactor model showed low risk of bias when a unidimensional model was assumed (Omega H = .92, explained common variance of .70). Fifteen item pairs (2%) were locally dependent. Five items showed poor scalability. All items fitted the IRT model; slope parameters ranged from .60 to 2.00, and threshold parameters from –2.05 to 6.80. One item showed DIF for age, 1 item DIF for gender, and 5 items showed DIF for language, but the impact on total scores was low. Our study shows limitations of the Dutch-Flemish Patient-Reported Outcomes Measurement Information System Pain Behavior item bank when used in a primary care population with musculoskeletal complaints. Perspective: We studied the psychometric properties of the Dutch-Flemish Patient-Reported Outcomes Measurement Information System Pain Behavior item bank in a large primary care population of patients with musculoskeletal complaints. It showed that the Pain Behavior item bank has limitations when used in this population.

Background and objective: The present study aimed to investigate the effects of selective calcitonin gene related peptide (CGRP) receptor antagonist (MK-8825) on cortical spreading depression (CSD) induced pain behavior and anxiety in freely-moving rats, and neuronal activation in the correlated anatomical regions. Methods: CSD was induced while keeping all meningeal layers and BBB intact and MK-8825 was administered in two different doses. Regional cerebral blood flow (rCBF), arterial pressure and DC shift were recorded. Behavioral studies were conducted in freely-moving rats. Spontaneous behavior, mechanical allodynia, ultrasonic vocalization, and anxiety were evaluated. Immunohistochemistry of c-fos, CGRP, calcitonin receptor like-receptor (CLR) and receptor activity modifying protein 1 (RAMP1) were studied. Results: MK-8825 did not block DC shifts in the cerebral cortex and accompanied hemodynamic response. CSD significantly induced freezing and grooming behavior in freely-moving rats. MK-8825 reversed increased episodes of freezing, grooming, wet dog shake and head shake behavior. MK-8825 increased CSD-induced reductions in von Frey thresholds, but did not change elevated plus maze results. MK-8825 blocked c-fos induction by CSD in the brainstem trigeminal nucleus caudalis (TNC) and reticular nucleus of thalamus (TRN) but not in the amygdala. Immunofluorescence analysis showed no co-localization of CGRP, CLR or RAMP1 with c-fos positive cells. Conclusion: CGRP receptor antagonist MK-8825 dose dependently attenuated CSD-induced trigeminal nerve mediated pain response without altering CSD waves and accompanied rCBF response. While blocking TNC activation, MK-8825 did not exert any effect on amygdala and anxiety behavior. CGRP receptor antagonists may also modulate thalamo-cortical gating.

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The distribution of prepronociceptin messenger RNA, the recently identified endogenous ligand of the ORL1 receptor (opioid receptor-like-1), has been studied in the adult mouse central nervous system using in situ hybridization. Prepronociceptin is a new peptide precursor that generates, upon maturation, at least three bioactive peptides: nociceptin, noc2 and the recently described nocistatin. Considering both the density of labeled neurons per region and their intensity of labeling, the distribution of prepronociceptin messenger RNA-containing neurons can be summarized as follows: the highest level of prepronociceptin messenger RNA expression was detected in the septohippocampal nucleus, bed nucleus of the stria terminalis, central amygdaloid nucleus, and in selective thalamic nuclei such as the parafascicular, reticular, ventral lateral geniculate and zona incerta. High to moderate levels of prepronociceptin messenger RNA expression were detected in the lateral, ventral and medial septum, and were evident in brainstem structures implicated in descending antinociceptive pathways (e.g. the gigantocellular nucleus, raphe magnus nucleus, periaqueductal gray matter), and also observed in association with auditory relay nuclei such as the inferior colliculi, lateral lemniscus nucleus, medioventral preolivary nucleus and lateral superior nucleus. A moderate level of prepronociceptin messenger RNA expression was observed in the medial preoptic nucleus, ventromedial preoptic nucleus, periventricular nucleus, pedonculopontine tegmental nucleus, solitary tract nucleus and spinal trigeminal nucleus. A weak level of prepronociceptin messenger RNA expression was present in some areas, such as the cerebral cortex, endopiriform cortex, hippocampal formation, medial amygdaloid nucleus, anterior hypothalamic area, medial mammillary hypothalamic nuclei, retrorubral field and substantia nigra pars compacta. No labeled cells could be found in the caudate-putamen, nucleus accumbens and, Journal Article, Research Support, Non-U.S. Gov't, info:eu-repo/semantics/published

The distribution of prepronociceptin messenger RNA, the recently identified endogenous ligand of the ORL1 receptor (opioid receptor-like-1), has been studied in the adult mouse central nervous system using in situ hybridization. Prepronociceptin is a new peptide precursor that generates, upon maturation, at least three bioactive peptides: nociceptin, noc2 and the recently described nocistatin. Considering both the density of labeled neurons per region and their intensity of labeling, the distribution of prepronociceptin messenger RNA-containing neurons can be summarized as follows: the highest level of prepronociceptin messenger RNA expression was detected in the septohippocampal nucleus, bed nucleus of the stria terminalis, central amygdaloid nucleus, and in selective thalamic nuclei such as the parafascicular, reticular, ventral lateral geniculate and zona incerta. High to moderate levels of prepronociceptin messenger RNA expression were detected in the lateral, ventral and medial septum, and were evident in brainstem structures implicated in descending antinociceptive pathways (e.g. the gigantocellular nucleus, raphe magnus nucleus, periaqueductal gray matter), and also observed in association with auditory relay nuclei such as the inferior colliculi, lateral lemniscus nucleus, medioventral preolivary nucleus and lateral superior nucleus. A moderate level of prepronociceptin messenger RNA expression was observed in the medial preoptic nucleus, ventromedial preoptic nucleus, periventricular nucleus, pedonculopontine tegmental nucleus, solitary tract nucleus and spinal trigeminal nucleus. A weak level of prepronociceptin messenger RNA expression was present in some areas, such as the cerebral cortex, endopiriform cortex, hippocampal formation, medial amygdaloid nucleus, anterior hypothalamic area, medial mammillary hypothalamic nuclei, retrorubral field and substantia nigra pars compacta. No labeled cells could be found in the caudate-putamen, nucleus accumbens and, Journal Article, Research Support, Non-U.S. Gov't, info:eu-repo/semantics/published

El objetivo del presente trabajo consiste en presentar los resultados sobre la evolución de la actividad EMG de los músculos frontales y sobre la relación entre los componentes del dolor, obtenidos en dos investigaciones en que aplicamos un procedimiento de BF EMG como tratamiento de las cefaleas tensionales. Dichos resultados, similares en ambos estudios, pueden resumirse del modo siguiente: a) Si bien la actividad EMG frontal durante las fases de biofeedback experimentó un decremento estadísticamente significativo a lo largo de las sesiones de tratamiento, también disminuyó significativamente el EMG frontal durante las fases de nivel basal previas; b) No se encontró una relación consistente entre los indicadores subjetivos de la cefalea (actividad, duración y frecuencia) y las conductas de dolor; y e) ambos componentes de la cefalea experimentaron un decremento significativo después de la intervención psicológica., In this paper we examine the results concerning frontal EMG evolution and the relationship between pain components of two studies where we applied an EMG biofeedback procedure as treatment for tension headache. These results can be summarized as follows: a) both frontal EMG during biofeedback phases and frontal EMG during previous baseline phases significantly decreased throughout treatment sessions; b) pain subjective indicators (activity, duration and frequency) and pain behaviors were not consistently related; and e) both two headache components -subjective and behavioral- significantly decreased after psychological intervention.

El objetivo del presente trabajo consiste en presentar los resultados sobre la evolución de la actividad EMG de los músculos frontales y sobre la relación entre los componentes del dolor, obtenidos en dos investigaciones en que aplicamos un procedimiento de BF EMG como tratamiento de las cefaleas tensionales. Dichos resultados, similares en ambos estudios, pueden resumirse del modo siguiente: a) Si bien la actividad EMG frontal durante las fases de biofeedback experimentó un decremento estadísticamente significativo a lo largo de las sesiones de tratamiento, también disminuyó significativamente el EMG frontal durante las fases de nivel basal previas; b) No se encontró una relación consistente entre los indicadores subjetivos de la cefalea (actividad, duración y frecuencia) y las conductas de dolor; y e) ambos componentes de la cefalea experimentaron un decremento significativo después de la intervención psicológica., In this paper we examine the results concerning frontal EMG evolution and the relationship between pain components of two studies where we applied an EMG biofeedback procedure as treatment for tension headache. These results can be summarized as follows: a) both frontal EMG during biofeedback phases and frontal EMG during previous baseline phases significantly decreased throughout treatment sessions; b) pain subjective indicators (activity, duration and frequency) and pain behaviors were not consistently related; and e) both two headache components -subjective and behavioral- significantly decreased after psychological intervention.