Articles: neuropathic-pain.
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Comparative Study
Are psychological predictors of chronic postsurgical pain dependent on the surgical model? A comparison of total knee arthroplasty and breast surgery for cancer.
Anxiety, depression, and catastrophizing are generally considered to be predictive of chronic postoperative pain, but this may not be the case after all types of surgery, raising the possibility that the results depend on the surgical model. We assessed the predictive value of these factors for chronic postsurgical pain in 2 different surgical models: total knee arthroplasty for osteoarthritis (89 patients, 65% women, age = 69 ± 9 years, baseline pain intensity = 4.7 ± 2.1) and breast surgery for cancer (100 patients, 100% women, age = 55 ± 12 years, no preoperative pain). Data were collected before surgery, then 2 days and 3 months after surgery. Anxiety, depression, and catastrophizing were measured with the Spielberger State-Trait Anxiety Inventory, Beck Depression Inventory, and Pain Catastrophizing Scale, respectively. Pain was assessed with the Brief Pain Inventory. Neuropathic pain was detected with the DN4 questionnaire. Multivariate logistic regression analyses for the total knee arthroplasty and breast surgery models considered together indicated that the presence of clinically meaningful chronic pain at 3 months (pain intensity ≥3/10) was predicted independently by age (P = .04), pain intensity on day 2 (P = .009), and state anxiety (P = .001). Linear regression models also showed that pain magnification, one of the dimensions of catastrophizing, independently predicted chronic pain intensity (P = .04). These results were not affected by the surgical model or by the neuropathic characteristics of the pain. Thus, state anxiety and pain magnification seem to constitute psychological risk factors for chronic postsurgical pain relevant in all surgical models. ⋯ This prospective study performed in patients with total knee arthroplasty or breast surgery for cancer shows that state anxiety, amplification of pain, and acute postoperative pain independently predict postsurgical pain at 3 months and that this does not depend on the surgical model.
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Ketogenic diets are well established as a successful anticonvulsant therapy. Based on overlap between mechanisms postulated to underlie pain and inflammation, and mechanisms postulated to underlie therapeutic effects of ketogenic diets, recent studies have explored the ability for ketogenic diets to reduce pain. Here we review clinical and basic research thus far exploring the impact of a ketogenic diet on thermal pain, inflammation, and neuropathic pain.
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In this study, the expression and functional role of metallothioneins I and II (MT-I/II) were evaluated in the spinal cord in rat models of inflammatory and neuropathic pain. Complete Freund's adjuvant (CFA) injection into the hindpaw induced an increase in MT-I/II protein expression in bilateral dorsal and ventral horns throughout the spinal cord, while chronic constriction injury (CCI) of the sciatic nerve induced an increase in MT-I/II expression in the ipsilateral dorsal and ventral horns of the lower lumbar spinal cord. ⋯ Treatment with MT-I siRNA before CFA injection or at early time points after CCI resulted in a significant attenuation of mechanical allodynia and thermal hyperalgesia, while treatment at later time points had no effect on established pain behaviors. Our results suggest that endogenous MT-I/II might play an important role in the pathogenesis of pain behaviors, participating in the initiation of inflammatory and neuropathic pain rather than in their maintenance.
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Neuropathic pain is a common chronic pain condition that can be challenging to treat, particularly for non-specialists. The development of the Map of Medicine care pathway for the management of neuropathic pain was led by the British Pain Society. Focusing on treatment by non-specialists, this pathway is based on new evidence, consensus, and the interests of service users. ⋯ Although the emphasis was not on specialist treatment, advice is given on existing interventions, including neural stimulation and multi-disciplinary care. These, and other steps on the pathway, will be subject to further review as more evidence becomes available. In the meantime, the pathway represents a straightforward, valuable and accessible approach for healthcare professionals managing the distress and impact of neuropathic pain.
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Inflammation is the process by which an organism responds to tissue injury involving both immune cell recruitment and mediator release. Diverse causes of neuropathic pain are associated with excessive inflammation in both the peripheral and central nervous system which may contribute to the initiation and maintenance of persistent pain. Chemical mediators, such as cytokines, chemokines, and lipid mediators, released during an inflammatory response have the undesired effect of sensitizing and stimulating nociceptors, their central synaptic targets or both. ⋯ This review aims to provide an overview of inflammatory mechanisms at differing levels of the sensory neuroaxis with a focus on neuropathic pain. We will compare and contrast neuropathic pain states such as traumatic nerve injury which is associated with a vigorous inflammatory response and chemotherapy induced pain in which the inflammatory response is much more modest. Targeting excessive inflammation in neuropathic pain provides potential therapeutic opportunities and we will discuss some of the opportunities but also the clinical challenges in such an approach.