Lee M.,Centers for Pain Management |
Silverman S.,Comprehensive Pain Medicine |
Hansen H.,The Pain Relief Centers |
Patel V.,ACMI Pain Care |
And 2 more authors.
Pain Physician | Year: 2011
Opioid-induced hyperalgesia (OIH) is defined as a state of nociceptive sensitization caused by exposure to opioids. The condition is characterized by a paradoxical response whereby a patient receiving opioids for the treatment of pain could actually become more sensitive to certain painful stimuli. The type of pain experienced might be the same as the underlying pain or might be different from the original underlying pain. OIH appears to be a distinct, definable, and characteristic phenomenon that could explain loss of opioid efficacy in some patients. Findings of the clinical prevalence of OIH are not available. However, several observational, cross-sectional, and prospective controlled trials have examined the expression and potential clinical significance of OIH in humans. Most studies have been conducted using several distinct cohorts and methodologies utilizing former opioid addicts on methadone maintenance therapy, perioperative exposure to opioids in patients undergoing surgery, and healthy human volunteers after acute opioid exposure using human experimental pain testing. The precise molecular mechanism of OIH, while not yet understood, varies substantially in the basic science literature, as well as clinical medicine. It is generally thought to result from neuroplastic changes in the peripheral and central nervous system (CNS) that lead to sensitization of pronociceptive pathways. While there are many proposed mechanisms for OIH, 5 mechanisms involving the central glutaminergic system, spinal dynorphins, descending facilitation, genetic mechanisms, and decreased reuptake and enhanced nociceptive response have been described as the important mechanisms. Of these, the central glutaminergic system is considered the most common possibility. Another is the hypothesis that N-methyl-D-aspartate (NMDA) receptors in OIH include activation, inhibition of the glutamate transporter system, facilitation of calcium regulated intracellular protein kinase C, and cross talk of neural mechanisms of pain and tolerance. Clinicians should suspect OIH when opioid treatment's effect seems to wane in the absence of disease progression, particularly if found in the context of unexplained pain reports or diffuse allodynia unassociated with the original pain, and increased levels of pain with increasing dosages. The treatment involves reducing the opioid dosage, tapering them off, or supplementation with NMDA receptor modulators. This comprehensive review addresses terminology and definition, prevalence, the evidence for mechanism and physiology with analysis of various factors leading to OIH, and effective strategies for preventing, reversing, or managing OIH.
Reddi D.,University College London |
Curran N.,Quail Surgical & Pain Management Center
Postgraduate Medical Journal | Year: 2014
Interest in chronic pain after surgery has grown since the finding that more than a fifth of patients attending chronic pain clinics cite surgery as the cause for their chronic pain. The problem is not limited to major surgery; even common minor procedures such as hernia repair have a significant risk of chronic pain. Surgical technique can influence the development of chronic postsurgical pain (CPSP) and techniques to minimise nerve injury should be used where possible. Central nervous system changes contribute to the development of persistent pain following surgical trauma and nerve injury. Pharmacological agents that interrupt the mechanisms contributing to central sensitisation may be helpful in reducing the incidence of CPSP. Psychosocial factors are also important in the development of chronic pain and should be addressed as part of a holistic approach to perioperative care.
Zhang J.,Zhengzhou University |
Ho K.-Y.,Quail Surgical & Pain Management Center |
Wang Y.,Zhengzhou University
British Journal of Anaesthesia | Year: 2011
Multimodal treatment of postoperative pain using adjuncts such as gabapentin is becoming more common. Pregabalin has anti-hyperalgesic properties similar to gabapentin. In this systematic review, we evaluated randomized, controlled trials (RCTs) for the analgesic efficacy and opioid-sparing effect of pregabalin in acute postoperative pain. A systematic search of Medline (1966-2010), the Cochrane Central Register of Controlled Trials (CENTRAL), and Google Scholar was performed. We identified 11 valid RCTs that used pregabalin for acute postoperative pain. Postoperative pain intensity was not reduced by pregabalin. Cumulative opioid consumption at 24 h was significantly decreased with pregabalin. At pregabalin doses of ≥300 mg, there was a reduction of 8.8 mg [weighted mean difference (WMD)]. At pregabalin doses <300 mg, cumulative opioid consumption was even lower (WMD, -13.4 mg). Pregabalin reduced opioid-related adverse effects such as vomiting [risk ratio (RR) 0.73; 95% confidence interval (CI) 0.56-0.95]. However, the risk of visual disturbance was greater (RR 3.29; 95% CI 1.95-5.57). Perioperative pregabalin administration reduced opioid consumption and opioid-related adverse effects after surgery. © The Author . Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved.
Goldschneider K.R.,Quail Surgical & Pain Management Center
Pain Research and Management | Year: 2012
BACKGROUND: Complex regional pain syndrome (CRPS) is a painful disorder without a known unifying mechanism. There are little data on which to base evaluation and treatment decisions, and what data are available come from studies involving adults; however, even that literature is relatively sparse. Developing robust research for CRPS in children is essential for the progress toward optimal treatment. OBJECTIVES: To determine potential avenues of research in pediatric CRPS based on a review of the literature. Areas of concern include diagnostic criteria, peripheral mechanisms, central nervous system mechanisms, the role of the autonomic nervous system, possible risk factors, options for prevention and potential avenues of treatment. METHODS: A literature review was performed and the results applied to form the hypotheses posited in the form of research questions. Results and CONCLUSIONS: CRPS is a complicated entity that is more than a painful sensory condition. There is evidence for peripheral inflammatory and neurological changes, and reorganization in both sensory and motor cortexes. In addition, a significant motor component is frequently observed and there appear to be tangible risk factors. Many of these pieces of evidence suggest options for prevention, treatment and monitoring progress and outcome. Most of the data are derived from adult studies and need to be replicated in children. Furthermore, there may be factors unique to pediatrics due to developmental changes in neuroplastic-ity as well as somatic, endocrinological and emotional growth. Some of these developmental factors may shed light on the adult condition. © 2012 Pulsus Group Inc.
Reddi D.,Quail Surgical & Pain Management Center
Anaesthesia | Year: 2016
Chronic postoperative pain is common. Nerve injury and inflammation promote chronic pain, the risk of which is influenced by patient factors, including psychological characteristics. Interventional trials to prevent chronic postoperative pain have been underpowered with inadequate patient follow-up. Ketamine may reduce chronic postoperative pain, although the optimum treatment duration and dose for different operations have yet to be identified. The evidence for gabapentin and pregabalin is encouraging but weak; further work is needed before these drugs can be recommended for the prevention of chronic pain. Regional techniques reduce the rates of chronic pain after thoracotomy and breast cancer surgery. Nerve-sparing surgical techniques may be of benefit, although nerve injury is not necessary or sufficient for chronic pain to develop. © 2015 The Association of Anaesthetists of Great Britain and Ireland.