Una revisión exhaustiva de la hiperalgesia inducida por opioides
A comprehensive review of opioid-induced hyperalgesia.
Lee M, Silverman SM, Hansen H, Patel VB, Manchikanti L.
Centers for Pain Management, Tifton, GA 31794, USA. info@centersforpain.com
Pain Physician. 2011 Mar-Apr;14(2):145-61.
Abstract
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 reviewaddresses 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.
http://www.painphysicianjournal.com/2011/march/2011;14;145-161.pdf
http://www.integration.samhsa.gov/pbhci-learning-community/Opioid-Induced_Hyperalgesia_Article.pdf
Hiperalgesia inducida por opioides: implicaciones clínicas para al algólogo.
Opioid induced hyperalgesia: clinical implications for the pain practitioner.
Silverman SM.
Comprehensive Pain Medicine, Pompano Beach, FL 33064, USA. silvpain1@bellsouth.net
Pain Physician. 2009 May-Jun;12(3):679-84.
Abstract
Opioids have been and continue to be used for the treatment of chronic pain. Evidence supports the notion that opioids can be safely administered in patients with chronic pain without the development of addiction or chemical dependency. However, over the past several years, concerns have arisen with respect to administration of opioids for the treatment of chronic pain, particularly non-cancer pain. Many of these involve legal issues with respect to diversion and prescription opioid abuse. Amongst these, opioid induced hyperalgesia (OIH) is becoming more prevalent as the population receiving opioids for chronic pain increases. OIH is a recognized complication of opioid therapy. It is a pro-nocioceptive process which is related to, but different from, tolerance. This focused review will elaborate on the neurobiological mechanisms of OIH as well as summarize the pre-clinical and clinical studies supporting the existence of OIH. In particular, the role of the excitatory neurotransmitter, N-methyl-D-aspartate appears to play a central, but not the only, role in OIH. Other mechanisms of OIH include the role of spinal dynorphins and descending facilitation from the rostral ventromedial medulla. The links between pain, tolerance, and OIH will be discussed with respect to their common neurobiology. Practical considerations for diagnosis and treatment for OIH will be discussed. It is crucial for the pain specialist to differentiate amongst clinically worsening pain, tolerance, and OIH since the treatment of these conditions differ. Tolerance is a necessary condition for OIH but the converse is not necessarily true. Office-based detoxification, reduction of opioid dose, opioid rotation, and the use of specific NMDA receptor antagonists are all viable treatment options for OIH. The role of sublingual buprenorphine appears to be an attractive, simple option for the treatment of OIH and is particularly advantageous for a busy interventional pain practice.
http://www.painphysicianjournal.com/2009/may/2009;12;679-684.pdf
Opioid-induced hyperalgesia
Hiperalgesia inducida por opioides (HIO)
Dr. Guillermo Aréchiga-Ornelas, Dr. José Emilio Mille-Loera, Dr. Alfonso Ramírez-Guerrero
Revista Mexicana de Anestesiología Volumen 33, Suplemento 1, abril-junio 2010
http://www.sld.cu/galerias/pdf/sitios/anestesiologia/hiperalgesia_y_opioides_2010.pdf
Hiperalgesia inducida por opioides (HIO)
Plínio da Cunha Leal, Jefferson Clivatti, João Batista Santos Garcia, Rioko Kimiko Sakata
Rev Bras Anestesiol 2010; 60: 6: 355-359
http://www.scielo.br/pdf/rba/v60n6/es_v60n6a11.pdf
Atentamente
Anestesiología y Medicina del Dolor
www.anestesia-dolor.org
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