A pain neuromatrix approach to patients with chronic pain

This paper presents an approach to rehabilitation of pain patients. The fundamental principles of the approach are (i) pain is an output of the brain that is produced whenever the brain concludes that body tissue is in danger and action is required, and (ii) pain is a multisystem output that is produced when an individual-specific cortical pain neuromatrix is activated. When pain becomes chronic, the efficacy of the pain neuromatrix is strengthened via nociceptive and non-nociceptive mechanisms, which means that less input, both nociceptive and non-nociceptive, is required to produce pain. The clinical approach focuses on decreasing all inputs that imply that body tissue is in danger and then on activating components of the pain neuromatrix without activating its output. Rehabilitation progresses to increase exposure to threatening input across sensory and non-sensory domains. (C) 2003 Elsevier Ltd. All rights reserved.

Experimental hand pain delays recognition of the contralateral hand: Evidence that acute and chronic pain have opposite effects on information processing?

Recognising the laterality of a pictured hand involves making an initial decision and confirming that choice by mentally moving one's own hand to match the picture. This depends on an intact body schema. Because patients with complex regional pain syndrome type 1 (CRPS1) take longer to recognise a hand's laterality when it corresponds to their affected hand, it has been proposed that nociceptive input disrupts the body schema. However, chronic pain is associated with physiological and psychosocial complexities that may also explain the results. In three studies, we investigated whether the effect is simply due to nociceptive input. Study one evaluated the temporal and perceptual characteristics of acute hand pain elicited by intramuscular injection of hypertonic saline into the thenar eminence. In studies two and three, subjects performed a hand laterality recognition task before, during, and after acute experimental hand pain, and experimental elbow pain, respectively. During hand pain and during elbow pain, when the laterality of the pictured hand corresponded to the painful side, there was no effect on response time (RT). That suggests that nociceptive input alone is not sufficient to disrupt the working body schema. Conversely to patients with CRPS1, when the laterality of the pictured hand corresponded to the non-painful hand, RT increased similar to 380 ms (95% confidence interval 190 ms-590 ms). The results highlight the differences between acute and chronic pain and may reflect a bias in information processing in acute pain toward the affected part.

mu O-conotoxin MrVIB selectively blocks Na(v)1.8 sensory neuron specific sodium channels and chronic pain behavior without motor deficits

The tetroclotoxin-resistant voltage-gated sodium channel (VGSC) Na(v)1.8 is expressed predominantly by damage-sensing primary afferent nerves and is important for the development and maintenance of persistent pain states. Here we demonstrate that mu O-conotoxin MrVIB from Conus marmoreus displays substantial selectivity for Na(v)1.8 and inhibits pain behavior in models of persistent pain. In rat sensory neurons, submicromolar concentrations of MrVIB blocked tetroclotoxin-resistant current characteristic of Na(v)1.8 but not Na(v)1.9 or tetroclotoxin-sensitive VGSC currents. MrVIB blocked human Nav1.8 expressed in Xenopus oocytes with selectivity at least 10-fold greater than other VGSCs. In neuropathic and chronic inflammatory pain models, allodynia and hyperalgesia were both reduced by intrathecal infusion of MrVIB (0.03-3 nmol), whereas motor side effects occurred only at 30-fold higher doses. In contrast, the nonselective VGSC blocker lignocaine displayed no selectivity for allodynia and hyperalgesia versus motor side effects. The actions of MrVIB reveal that VGSC antagonists displaying selectivity toward Na(v)1.8 can alleviate chronic pain behavior with a greater therapeutic index than nonselective antagonists.

Core stability exercise in chronic low back pain

Exercise is commonly used in the management of chronic musculoskeletal conditions, including chronic low back pain (CLBP). The focus of exercise is varied and may include parameters ranging from strength and endurance training, to specific training of muscle coordination and control. The assumption underpinning these approaches is that improved neuromuscular function will restore or augment the control and support of the spine and pelvis. In a biomechanical model of CLBP, which assumes that pain recurrence is caused by repeated mechanical irritation of pain sensitive structures [1], it is proposed that this improved control and stability would reduce mechanical irritation and lead to pain relief [1]. Although this model provides explanation for the chronicity of LBP, perpetuation of pain is more complex, and contemporary neuroscience holds the view that chronic pain is mediated by a range of changes including both peripheral (eg, peripheral sensitization) and central neuroplastic changes [2]. Although this does not exclude the role of improved control of the lumbar spine and pelvis in management of CLBP, particularly when there is peripheral sensitization, it highlights the need to look beyond outdated simplistic models. One factor that this information highlights is that the refinement of control and coordination may be more important than simple strength and endurance training for the trunk muscles. The objective of this article is to discuss the rationale for core stability exercise in the management of CLBP, to consider critical factors for its implementation, and to review evidence for efficacy of the approach.

The relationship of adult attachment to emotion, catastrophizing, control, threshold and tolerance, in experimentally-induced pain

Although insecure attachment has been associated with a range of variables linked with problematic adjustment to chronic pain, the causal direction of these relationships remains unclear. Adult attachment style is, theoretically, developmentally antecedent to cognitions, emotions and behaviours (and might therefore be expected to contribute to maladjustment). It can also be argued, however, that the experience of chronic pain increases attachment insecurity. This project examined this issue by determining associations between adult attachment characteristics, collected prior to an acute (coldpressor) pain experience, and a range of emotional, cognitive, pain tolerance, intensity and threshold variables collected during and after the coldpressor task. A convenience sample of 58 participants with no history of chronic pain was recruited. Results demonstrated that attachment anxiety was associated with lower pain thresholds; more stress, depression, and catastrophizing; diminished perceptions of control over pain; and diminished ability to decrease pain. Conversely, secure attachment was linked with lower levels of depression and catastrophizing, and more control over pain. Of particular interest were findings that attachment style moderated the effects of pain intensity on the tendency to catastrophize, such that insecurely attached individuals were more likely to catastrophize when reporting high pain intensity. This is the first study to link attachment with perceptions of pain in a pain-free sample. These findings cast anxious attachment as a vulnerability factor for chronic pain following acute episodes of pain, while secure attachment may provide more resilience. (c) 2006 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.