Role of attentional focus in pain perception: Manipulation of response to noxious stimulation by instructions.

1971 ◽  
Vol 77 (1) ◽  
pp. 42-45 ◽  
Author(s):  
Bernard Blitz ◽  
Albert J. Dinnerstein
Author(s):  
Pierluigi Diotaiuti ◽  
Stefano Corrado ◽  
Stefania Mancone ◽  
Lavinia Falese ◽  
Angelo Rodio ◽  
...  

Background. Recently, a growing interest has emerged in the role of attention and hypervigilance in the experience of pain. Shifting attention away from pain seems likely to reduce the perception of pain itself. Objectives. The present study has been designed to test the following overall hypotheses: (1) disposition to catastrophize, self-efficacy perceived in pain resistance (task self-efficacy), previous experiences concerning the tolerance of physical pain, and degree of impulsiveness are significant predictors of the decision to abandon a painful test such as the cold pressor test (CPT); (2) the manipulation of the attentive focus (internal or external) can influence the level of perceived pain. Methods. Effects of the manipulation of attentional focus (internal and external) on pain perception and response of trial abandonment were evaluated in a sample of university students (n = 246) subjected to the cold pressor test. Results. A significant effect (p < 0.05) was found through a test–retest comparison on the final level of perceived pain among subjects who had received instruction to externalize the focus of their attention (mixed factorial analysis of variance), but no significance was observed with respect to the decision to abandon the experiment. A general explanatory model of the abandonment behavior demonstrating overall good fit measurements was tested too. Conclusion. The abandonment of tests has been shown to be predicted mainly by catastrophic attitude. Attentive impulsiveness showed a further positive effect on catastrophic attitude. Perceived self-efficacy in the tolerance of pain limited learned helplessness, which in turn positively influenced catastrophizing.


2013 ◽  
Vol 18 (1) ◽  
pp. 1-18 ◽  
Author(s):  
Robert J. Barth

Abstract Scientific findings have indicated that psychological and social factors are the driving forces behind most chronic benign pain presentations, especially in a claim context, and are relevant to at least three of the AMA Guides publications: AMA Guides to Evaluation of Disease and Injury Causation, AMA Guides to Work Ability and Return to Work, and AMA Guides to the Evaluation of Permanent Impairment. The author reviews and summarizes studies that have identified the dominant role of financial, psychological, and other non–general medicine factors in patients who report low back pain. For example, one meta-analysis found that compensation results in an increase in pain perception and a reduction in the ability to benefit from medical and psychological treatment. Other studies have found a correlation between the level of compensation and health outcomes (greater compensation is associated with worse outcomes), and legal systems that discourage compensation for pain produce better health outcomes. One study found that, among persons with carpal tunnel syndrome, claimants had worse outcomes than nonclaimants despite receiving more treatment; another examined the problematic relationship between complex regional pain syndrome (CRPS) and compensation and found that cases of CRPS are dominated by legal claims, a disparity that highlights the dominant role of compensation. Workers’ compensation claimants are almost never evaluated for personality disorders or mental illness. The article concludes with recommendations that evaluators can consider in individual cases.


2007 ◽  
Author(s):  
Jeffrey I. Gold ◽  
Trina Haselrig ◽  
D. Colette Nicolaou ◽  
Katharine A. Belmont

Author(s):  
Floriana Costanzo ◽  
Elisa Fucà ◽  
Deny Menghini ◽  
Antonella Rita Circelli ◽  
Giovanni Augusto Carlesimo ◽  
...  

Event-based prospective memory (PM) was investigated in children with Attention deficit/hyperactivity disorder (ADHD), using a novel experimental procedure to evaluate the role of working memory (WM) load, attentional focus, and reward sensitivity. The study included 24 children with ADHD and 23 typically-developing controls. The experimental paradigm comprised one baseline condition (BC), only including an ongoing task, and four PM conditions, varying for targets: 1 Target (1T), 4 Targets (4T), Unfocal (UN), and Reward (RE). Children with ADHD were slower than controls on all PM tasks and less accurate on both ongoing and PM tasks on the 4T and UN conditions. Within the ADHD group, the accuracy in the RE condition did not differ from BC. A significant relationship between ADHD-related symptoms and reduced accuracy/higher speed in PM conditions (PM and ongoing trials), but not in BC, was detected. Our data provide insight on the adverse role of WM load and attentional focus and the positive influence of reward in the PM performance of children with ADHD. Moreover, the relation between PM and ADHD symptoms paves the road for PM as a promising neuropsychological marker for ADHD diagnosis and intervention.


1999 ◽  
Vol 91 (1) ◽  
pp. 231-239 ◽  
Author(s):  
Uta S. Muth-Selbach ◽  
Irmgard Tegeder ◽  
Kay Brune ◽  
Gerd Geisslinger

Background Prostaglandin play a pivotal role in spinal nociceptive processing. At therapeutic concentrations, acetaminophen is not a cyclooxygenase inhibitor. inhibitor. Thus, it is antinociceptive without having antiinflammatory or gastrointestinal toxic effects. This study evaluated the role of spinal prostaglandin E2 (PGE2) in antinociception produced by intraperitoneally administered acetaminophen. Methods The PGE2 concentrations in the dorsal horn of the spinal cord were measured after formalin was injected into the hind paw of rats. The effect of antinociceptive doses of acetaminophen (100, 200, and 300 mg/kg given intraperitoneally) on PGE2 levels and flinching behavior was monitored Spinal PGE2 and acetaminophen concentrations were obtained by microdialysis using a probe that was implanted transversely through the dorsal horn of the spinal cord at L4. Furthermore, the effects of acetaminophen on urinary prostaglandin excretion were determined. Results Intraperitoneal administration of acetaminophen resulted in a significant decrease in spinal PGE2 release that was associated with a significant reduction in the flinching behavior in the formalin test Acetaminophen was distributed rapidly into the spinal cord with maximum dialysate concentrations 4560 min after intraperitoneal administration. Urinary excretion of prostanoids (PGE2, PGF2alpha, and 6-keto-PGF1alpha) was not significantly altered after acetaminophen administration. Conclusions The data confirm the importance of PGE2 in spinal nociceptive processing. The results suggest that antinociception after acetaminophen administration is mediated, at least in part, by inhibition of spinal PGE2 release. The mechanism, however, remains unknown. The finding that urinary excretion of prostaglandins was not affected might explain why acetaminophen is antinociceptive but does not compromise renal safety.


2009 ◽  
Vol 106 (1) ◽  
pp. 105-112 ◽  
Author(s):  
Marie K. Hoeger Bement ◽  
Rebecca L. Rasiarmos ◽  
John M. DiCapo ◽  
Audrey Lewis ◽  
Manda L. Keller ◽  
...  

2007 ◽  
Vol 69 (7) ◽  
pp. 1162-1174 ◽  
Author(s):  
Lisa N. Jefferies ◽  
Shahab Ghorashi ◽  
Jun-Ichiro Kawahara ◽  
Vincent tDi Lollo

2021 ◽  
Vol 12 ◽  
Author(s):  
Roberta Lattanzi ◽  
Cinzia Severini ◽  
Daniela Maftei ◽  
Luciano Saso ◽  
Aldo Badiani

The prokineticin (PK) family, prokineticin 1 and Bv8/prokineticin 2 (PROK2), initially discovered as regulators of gastrointestinal motility, interacts with two G protein-coupled receptors, PKR1 and PKR2, regulating important biological functions such as circadian rhythms, metabolism, angiogenesis, neurogenesis, muscle contractility, hematopoiesis, immune response, reproduction and pain perception. PROK2 and PK receptors, in particular PKR2, are widespread distributed in the central nervous system, in both neurons and glial cells. The PROK2 expression levels can be increased by a series of pathological insults, such as hypoxia, reactive oxygen species, beta amyloid and excitotoxic glutamate. This suggests that the PK system, participating in different cellular processes that cause neuronal death, can be a key mediator in neurological/neurodegenerative diseases. While many PROK2/PKRs effects in physiological processes have been documented, their role in neuropathological conditions is not fully clarified, since PROK2 can have a double function in the mechanisms underlying to neurodegeneration or neuroprotection. Here, we briefly outline the latest findings on the modulation of PROK2 and its cognate receptors following different pathological insults, providing information about their opposite neurotoxic and neuroprotective role in different pathological conditions.


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