No pain no gain? Pursuing a competing goal inhibits avoidance behavior.
Pain. 2012 Jan 31;
Authors: Van Damme S, Van Ryckeghem DM, Wyffels F, Van Hulle L, Crombez G
Abstract
This experiment investigated pain-related avoidance behavior in context of competing goals. Participants (N=56) were presented trials of 2 different tasks of which 1 task could produce pain. They were free to decide whether or not to perform trials of these tasks. In half of the participants, a competing goal was activated by instructing them that they would receive a monetary reward corresponding to the number of pain task trials actually performed (competition group). In the other half of the participants, no competing goal was installed (control group). Results showed that the competition group showed less frequent avoidance behavior than the control group. Furthermore, the association between pain-related avoidance behavior and fear of pain was smaller in the competition group than in the control group. The findings indicate that the emergence of pain-related avoidance behavior depends upon the motivational context, and that the association between pain-related fear and avoidance is not stable. This study has implications for our understanding of disability, and points to the need to consider avoidance behavior within a broad context of multiple, often competing, goals.
PMID: 22301333 [PubMed - as supplied by publisher]
Calcium/calmodulin dependent kinase II contributes to persistent central neuropathic pain following spinal cord injury.
Pain. 2012 Jan 30;
Authors: Crown ED, Gwak YS, Ye Z, Yu Tan H, Johnson KM, Xu GY, McAdoo DJ, Hulsebosch CE
Abstract
Chronic central neuropathic pain after central nervous system injuries remains refractory to therapeutic interventions. A novel approach would be to target key intracellular signaling proteins that are known to contribute to continued activation by phosphorylation of kinases, transcription factors, and/or receptors that contribute to changes in membrane excitability. We demonstrate that one signaling kinase, calcium/calmodulin-dependent kinase II (CaMKII), is critical in maintaining aberrant dorsal horn neuron hyperexcitability in the neuropathic pain condition after spinal cord injury (SCI). After contusion SCI at spinal level T10, activated CaMKII (phosphorylated, pCaMKII) expression is significantly upregulated in the T7/8 spinal dorsal horn in neurons, but not glial cells, and in oligodendrocytes in the dorsal column in the same rats that displayed at-level mechanical allodynia. Furthermore, identified spinothalamic neurons demonstrated significant increases of pCaMKII after SCI compared to sham-treated control animals. However, neither astrocytes nor microglia showed pCaMKII expression in either sham-treated or SCI rats. To demonstrate causality, treatment of SCI rats with KN-93, which prevents CaMKII activation, significantly attenuated at-level mechanical allodynia and aberrant wide dynamic range neuronal activity evoked by brush, pressure, and pinch stimuli and a graded series of von Frey stimuli, respectively. Persistent CaMKII activation contributes to chronic central neuropathic pain by mechanisms that involve maintained hyperexcitability of wide dynamic range dorsal horn neurons. Furthermore, targeting key signaling proteins is a novel, useful therapeutic strategy for treating chronic central neuropathic pain.
PMID: 22296735 [PubMed - as supplied by publisher]
Impact of parental catastrophizing and contextual threat on parents’ emotional and behavioral responses to their child’s pain.
Pain. 2012 Jan 22;
Authors: Caes L, Vervoort T, Trost Z, Goubert L
Abstract
Limited research has addressed processes underlying parents’ empathic responses to their child’s pain. The present study investigated the effects of parental catastrophizing, threatening information about the child’s pain, and child pain expression upon parental emotional and behavioral responses to their child’s pain. A total of 56 school children participated in a heat pain task consisting of 48 trials while being observed by 1 of their parents. Trials were preceded by a blue or yellow circle, signaling possible pain stimulation (i.e., pain signal) or no pain stimulation (i.e., safety signal). Parents received either neutral or threatening information regarding the heat stimulus. Parents’ negative emotional responses when anticipating their child’s pain were assessed using psychophysiological measures- i.e., fear-potentiated startle and corrugator EMG activity. Parental behavioral response to their child’s pain (i.e., pain attending talk) was assessed during a 3-minute parent-child interaction that followed the pain task. The Child Facial Coding System (CFCS) was used to assess children’s facial pain expression during the pain task. Results indicated that receiving threatening information was associated with a stronger parental corrugator EMG activity during pain signals in comparison with safety signals. The same pattern was found for parental fear-potentiated startle reflex, particularly when the child’s facial pain expression was high. In addition, parents who reported high levels of catastrophizing thought about their child’s pain engaged, in comparison with low-catastrophizing parents, in more pain-attending talk when they received threatening information. The findings are discussed in the context of affective-motivational theories of pain.
PMID: 22273548 [PubMed - as supplied by publisher]
Insomnia, sleep quality, pain, and somatic symptoms: sex differences and shared genetic components.
Pain. 2012 Jan 23;
Authors: Zhang J, Lam SP, Li SX, Tang NL, Yu MW, Li AM, Wing YK
Abstract
This study investigated the sex differences, and the shared genetic and environmental factors underlying the associations of sleep disturbances (insomnia and sleep quality) with pain and somatic symptoms in both adolescents and middle-aged adults. We recruited 259 adolescents (69 with current insomnia) and their parents (256 middle-aged adults, 78 with current insomnia). Insomnia severity and sleep quality were measured by the Insomnia Severity Inventory (ISI) and Pittsburgh Sleep Quality Index (PSQI), respectively. Pain and somatic symptoms were measured by the Somatic Symptom Inventory and Visual Analogue Scale for overall pain. Subjects with insomnia scored higher on all measures of pain and somatic symptoms than non-insomnia patients, in both adolescents and adults (P<.001). Both pain and somatic measures were associated with ISI and PSQI scores after controlling for age, sex, depressive and anxiety symptoms. There was an interaction effect between insomnia and female sex on pain and somatic symptoms (P<.05), especially in adults. Pain and somatic symptoms ran in family with moderate heritability (range h(2)=0.15-0.42). The phenotypic associations of ISI and PSQI with pain and somatic measures were both contributed by genetic (range p(G)=0.41-0.96) and environmental (range p(E)=0.27-0.40) factors with a major genetic contribution. In summary, insomnia and poor sleep quality are closely associated with pain and somatic symptoms. Insomnia seems to modulate the sex differences in pain and somatic symptoms, especially in the adult population. A shared genetic predisposition might underlie the associations of insomnia and sleep quality with pain and somatic symptoms.
PMID: 22277557 [PubMed - as supplied by publisher]
Dependence scores predict prognosis of medication overuse headache: a prospective cohort from the Akershus study of chronic headache.
Pain. 2012 Jan 24;
Authors: Lundqvist C, Grande RB, Aaseth K, Russell MB
Abstract
Medication overuse headache (MOH) is a chronic headache that is common in the general population. It has characteristics similar to drug dependence, and detoxification is established as the main treatment. The majority of MOH cases are in contact with general practitioners. Our objective was to investigate whether the Severity of Dependence Scale (SDS) score could be used as predictor for the prognosis of MOH in the general population. In a cross-sectional epidemiological survey, an age- and gender-stratified sample of 30,000 persons 30 to 44 years of age was recruited via a posted questionnaire. Those individuals with self-reported chronic headache (⩾15 days per month) were interviewed by neurological residents at Akershus University Hospital, Oslo. The International Classification of Headache Disorders was used. Those with MOH were re-interviewed by telephone 2 to 3 years after the initial interview. SDS scores and medication information were collected at baseline and follow-up. The main outcomes were SDS scores, termination of MOH and chronic headache from baseline to follow-up. We found the predominant overused analgesics in this sample to be simple analgesics. At follow-up, 65% of participants no longer had medication overuse, and 37% had changed to episodic headache (<15 days per month). The SDS score at baseline successfully predicted improvement for primary MOH, but not secondary MOH. The SDS scores decreased slightly from baseline to follow-up in those who stopped medication overuse, but were still significantly higher than in subjects with chronic headache without medication overuse at baseline. We conclude that the SDS score can predict successful prognosis related to detoxification of primary MOH but not in secondary MOH.
PMID: 22281099 [PubMed - as supplied by publisher]
Is there a potential role for attention bias modification in pain patients? Results of 2 randomised, controlled trials.
Pain. 2012 Jan 24;
Authors: Sharpe L, Ianiello M, Dear BF, Nicholson Perry K, Refshauge K, Nicholas MK
Abstract
Potential applications of attention bias modification (ABM) for acute and chronic pain patients are investigated. In study 1, 54 acute back pain patients (46 of whom completed the study) were recruited at their initial physiotherapy session and randomised to receive 1 session of ABM or placebo. Patients were followed up 3months later. Participants who were randomised to receive ABM reported less average (P=0.001) and current pain (P=0.008) and experienced pain for fewer days (P=0.01) than those who received placebo. In study 2, 34 chronic pain patients were recruited and randomly assigned to receive either 4 sessions of ABM (n=22) or placebo (n=12), followed by 8 sessions of cognitive behavioural treatment (CBT). After ABM, there was a significant group-by-time effect for disability. By 6-month follow-up, differences had emerged between the 2 training groups, such that the ABM group had shown greater reductions in anxiety sensitivity and disability than the placebo group. Although the results of these studies show that there is potential in the application of ABM to pain conditions, the mechanisms of treatment could not be established. Neither group showed an initial bias towards the word stimuli or a training effect, and only in the acute pain group were changes in biases related to outcome. Nonetheless, the fact that 2 independent samples showed a positive effect of ABM on clinical outcomes suggests that ABM is worthy of future study as an intervention for pain patients.
PMID: 22281100 [PubMed - as supplied by publisher]
Which domains should be included in a cancer pain classification system? Analyses of longitudinal data.
Pain. 2012 Jan 19;
Authors: Knudsen AK, Brunelli C, Klepstad P, Aass N, Apolone G, Corli O, Montanari M, Caraceni A, Kaasa S
Abstract
The overall aim of the present study was to further develop an evidence-based platform for the content of an international cancer pain classification system. Data from a multicentre, observational longitudinal study of cancer patients were analysed. Analyses were carried out in 2 samples: (A) Cross-sectional data of patients on opioids at inclusion, and (B) patients just admitted to palliative care. Outcome measures in the models we investigated were pain on average, worst pain, and pain relief at inclusion, and at day 14, respectively. Uni- and multivariate regression models were applied to test the explicative power on pain outcomes of a series of known pain domains, including incident pain, psychological distress, neuropathic pain, pain localisation, sleep disturbances, total morphine equivalent daily dose (MEDD), and cancer diagnosis. In the 2 analyses, 1529 (A) and 352 (B) patients were included, respectively. Incident pain, pain localisation, MEDD, use of nonsteroidal antiinflammatory drugs, and sleep were associated with one or more of the pain outcomes in analysis A, while initial pain intensity, initial pain relief, incident pain, localisation of pain, cancer diagnosis, and age were predictors in the longitudinal analysis. Identified domains explained 16% to 24% of the variability of the pain outcome. Initial pain intensity emerged as the strongest predictor of pain outcome after 2weeks, and incident pain was confirmed to be a relevant domain. The regression models explained only a minor part of the variability of pain outcomes.
PMID: 22264677 [PubMed - as supplied by publisher]
Acute experimental endotoxemia induces visceral hypersensitivity and altered pain evaluation in healthy humans.
Pain. 2012 Jan 18;
Authors: Benson S, Kattoor J, Wegner A, Hammes F, Reidick D, Grigoleit JS, Engler H, Oberbeck R, Schedlowski M, Elsenbruch S
Abstract
Growing evidence suggests that systemic immune activation plays a role in the pathophysiology of pain in functional bowel disorders. By implementing a randomized crossover study with an injection of endotoxin or saline, we aimed to test the hypothesis that endotoxin-induced systemic inflammation increases visceral pain sensitivity in humans. Eleven healthy men (mean±standard error of the mean age 26.6±1.1 years) received an intravenous injection of either lipopolysaccharide (LPS; 0.4ng/kg) or saline on 2 otherwise identical study days. Blood samples were collected 15min before and 1, 2, 3, 4, and 6h after injection to characterize changes in immune parameters including proinflammatory cytokines. Rectal sensory and pain thresholds and subjective pain ratings were assessed with barostat rectal distensions 2h after injection. LPS administration induced an acute inflammatory response indicated by transient increases in tumor necrosis factor alpha, interleukin 6, and body temperature (all P<.001). The LPS-induced immune activation increased sensitivity to rectal distensions as reflected by significantly decreased visceral sensory and pain thresholds (both P<.05) compared to saline control. Visceral stimuli were rated as more unpleasant (P<.05) and inducing increased urge to defecate (P<.01). Pain thresholds correlated with interleukin 6 at +1h (r=0.60, P<.05) and +3h (r=0.67, P<.05) within the LPS condition. This report is novel in that it demonstrates that a transient systemic immune activation results in decreased visceral sensory and pain thresholds and altered subjective pain ratings. Our results support the relevance of inflammatory processes in the pathophysiology of visceral hyperalgesia and underscore the need for studies to further elucidate immune-to-brain communication pathways in gastrointestinal disorders.
PMID: 22264996 [PubMed - as supplied by publisher]
Metallothionein deficiency in the injured peripheral nerves of complex regional pain syndrome as revealed by proteomics.
Pain. 2012 Jan 14;
Authors: Oki G, Wada T, Iba K, Aiki H, Sasaki K, Imai SI, Sohma H, Matsumoto K, Yamaguchi M, Fujimiya M, Yamashita T, Kokai Y
Abstract
Complex regional pain syndrome (CRPS) is characterized by persistent and severe pain after trauma or surgery; however, its molecular mechanisms in the peripheral nervous system are poorly understood. Using proteomics, we investigated whether injured peripheral nerves of CRPS patients have altered protein profiles compared with control nerves. We obtained nerve samples from 3 patients with CRPS-2 who underwent resection of part of an injured peripheral nerve. Sural nerves from fresh cadavers with no history of trauma or neuropathic pain served as controls. Proteomic analysis showed that the number and functional distribution of proteins expressed in CRPS and control nerves was similar. Interestingly, metallothionein was absent in the injured nerves of CRPS-2, although it was readily detected in control nerves. Western blotting further confirmed the absence of metallothionein in CRPS-2 nerves, and immunohistochemistry corroborated the deficiency of metallothionein expression in injured nerves from 5 of 5 CRPS patients and 2 of 2 patients with painful neuromas. In contrast, all control nerves, including 5 sural nerves from fresh cadavers and 41 nerves obtained from surgically resected tumors, expressed MT. Furthermore, expression of S100 as a marker for Schwann cells, and neurofilament M as a marker of axons was comparable in both CRPS-2 and controls. Metallothioneins are zinc-binding proteins that are probably involved in protection against injury and subsequent regeneration after CNS damage. Their absence from the injured peripheral nerves of patients with CRPS-2 suggests a potential pathogenic role in generating pain in the damaged peripheral nerves.
PMID: 22249007 [PubMed - as supplied by publisher]
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