Psychosocial factors predict opioid analgesia through endogenous opioid function.
Identifieur interne : 000C74 ( Main/Corpus ); précédent : 000C73; suivant : 000C75Psychosocial factors predict opioid analgesia through endogenous opioid function.
Auteurs : John W. Burns ; Stephen Bruehl ; Christopher R. France ; Erik Schuster ; Daria Orlowska ; Asokumar Buvanendran ; Melissa Chont ; Rajnish K. GuptaSource :
- Pain [ 1872-6623 ] ; 2017.
English descriptors
- KwdEn :
- Administration, Intravenous (MeSH), Adult (MeSH), Analgesics, Opioid (administration & dosage), Catastrophization (chemically induced), Catastrophization (psychology), Chronic Pain (drug therapy), Chronic Pain (psychology), Cross-Over Studies (MeSH), Double-Blind Method (MeSH), Female (MeSH), Humans (MeSH), Low Back Pain (drug therapy), Low Back Pain (psychology), Male (MeSH), Middle Aged (MeSH), Mood Disorders (chemically induced), Morphine (administration & dosage), Naloxone (administration & dosage), Narcotic Antagonists (administration & dosage), Pain Measurement (MeSH), Pain Threshold (drug effects), Pain Threshold (physiology), Psychiatric Status Rating Scales (MeSH), Self Report (MeSH).
- MESH :
- chemical , administration & dosage : Analgesics, Opioid, Morphine, Naloxone, Narcotic Antagonists.
- chemically induced : Catastrophization, Mood Disorders.
- drug effects : Pain Threshold.
- drug therapy : Chronic Pain, Low Back Pain.
- physiology : Pain Threshold.
- psychology : Catastrophization, Chronic Pain, Low Back Pain.
- Administration, Intravenous, Adult, Cross-Over Studies, Double-Blind Method, Female, Humans, Male, Middle Aged, Pain Measurement, Psychiatric Status Rating Scales, Self Report.
Abstract
Use of opioid analgesics for management of chronic nonmalignant pain has become common, yet there are presently no well-validated predictors of optimal opioid analgesic efficacy. We examined whether psychosocial factors (eg, depressive symptoms) predicted changes in spontaneous low back pain after administration of opioid analgesics, and whether endogenous opioid (EO) function mediated these relationships. Participants with chronic low back pain but who were not chronic opioid users (N = 89) underwent assessment of low back pain intensity pre- and post-drug in 3 (counterbalanced) conditions: (1) placebo, (2) intravenous naloxone, and (3) intravenous morphine. Comparison of placebo condition changes in back pain intensity to those under naloxone and morphine provided indexes of EO function and opioid analgesic responses, respectively. Results showed that (1) most psychosocial variables were related significantly and positively to morphine analgesic responses for low back pain, (2) depressive symptoms, trait anxiety, pain catastrophizing, and pain disability were related negatively to EO function, and (3) EO function was related negatively to morphine analgesic responses for low back pain. Bootstrapped mediation analyses showed that links between morphine analgesic responses and depressive symptoms, trait anxiety, pain catastrophizing, and perceived disability were partially mediated by EO function. Results suggest that psychosocial factors predict elevated analgesic responses to opioid-based medications, and may serve as markers to identify individuals who benefit most from opioid therapy. Results also suggest that people with greater depressive symptoms, trait anxiety, pain catastrophizing, and perceived disability may have deficits in EO function, which may predict enhanced response to opioid analgesics.
DOI: 10.1097/j.pain.0000000000000768
PubMed: 27898491
PubMed Central: PMC7176103
Links to Exploration step
pubmed:27898491Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Psychosocial factors predict opioid analgesia through endogenous opioid function.</title><author><name sortKey="Burns, John W" sort="Burns, John W" uniqKey="Burns J" first="John W" last="Burns">John W. Burns</name><affiliation><nlm:affiliation>Department of Behavioral Sciences, Rush University Medical Center, Chicago, IL USA.</nlm:affiliation></affiliation></author><author><name sortKey="Bruehl, Stephen" sort="Bruehl, Stephen" uniqKey="Bruehl S" first="Stephen" last="Bruehl">Stephen Bruehl</name><affiliation><nlm:affiliation>Department of Anesthesiology, Vanderbilt University School of Medicine, Vanderbilt, TN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="France, Christopher R" sort="France, Christopher R" uniqKey="France C" first="Christopher R" last="France">Christopher R. France</name><affiliation><nlm:affiliation>Department of Psychology, Ohio University, Athens, OH, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Schuster, Erik" sort="Schuster, Erik" uniqKey="Schuster E" first="Erik" last="Schuster">Erik Schuster</name><affiliation><nlm:affiliation>Department of Behavioral Sciences, Rush University Medical Center, Chicago, IL USA.</nlm:affiliation></affiliation></author><author><name sortKey="Orlowska, Daria" sort="Orlowska, Daria" uniqKey="Orlowska D" first="Daria" last="Orlowska">Daria Orlowska</name><affiliation><nlm:affiliation>Department of Behavioral Sciences, Rush University Medical Center, Chicago, IL USA.</nlm:affiliation></affiliation></author><author><name sortKey="Buvanendran, Asokumar" sort="Buvanendran, Asokumar" uniqKey="Buvanendran A" first="Asokumar" last="Buvanendran">Asokumar Buvanendran</name><affiliation><nlm:affiliation>Department of Behavioral Sciences, Rush University Medical Center, Chicago, IL USA.</nlm:affiliation></affiliation></author><author><name sortKey="Chont, Melissa" sort="Chont, Melissa" uniqKey="Chont M" first="Melissa" last="Chont">Melissa Chont</name><affiliation><nlm:affiliation>Department of Anesthesiology, Vanderbilt University School of Medicine, Vanderbilt, TN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Gupta, Rajnish K" sort="Gupta, Rajnish K" uniqKey="Gupta R" first="Rajnish K" last="Gupta">Rajnish K. Gupta</name><affiliation><nlm:affiliation>Department of Anesthesiology, Vanderbilt University School of Medicine, Vanderbilt, TN, USA.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:27898491</idno><idno type="pmid">27898491</idno><idno type="doi">10.1097/j.pain.0000000000000768</idno><idno type="pmc">PMC7176103</idno><idno type="wicri:Area/Main/Corpus">000C74</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000C74</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Psychosocial factors predict opioid analgesia through endogenous opioid function.</title><author><name sortKey="Burns, John W" sort="Burns, John W" uniqKey="Burns J" first="John W" last="Burns">John W. Burns</name><affiliation><nlm:affiliation>Department of Behavioral Sciences, Rush University Medical Center, Chicago, IL USA.</nlm:affiliation></affiliation></author><author><name sortKey="Bruehl, Stephen" sort="Bruehl, Stephen" uniqKey="Bruehl S" first="Stephen" last="Bruehl">Stephen Bruehl</name><affiliation><nlm:affiliation>Department of Anesthesiology, Vanderbilt University School of Medicine, Vanderbilt, TN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="France, Christopher R" sort="France, Christopher R" uniqKey="France C" first="Christopher R" last="France">Christopher R. France</name><affiliation><nlm:affiliation>Department of Psychology, Ohio University, Athens, OH, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Schuster, Erik" sort="Schuster, Erik" uniqKey="Schuster E" first="Erik" last="Schuster">Erik Schuster</name><affiliation><nlm:affiliation>Department of Behavioral Sciences, Rush University Medical Center, Chicago, IL USA.</nlm:affiliation></affiliation></author><author><name sortKey="Orlowska, Daria" sort="Orlowska, Daria" uniqKey="Orlowska D" first="Daria" last="Orlowska">Daria Orlowska</name><affiliation><nlm:affiliation>Department of Behavioral Sciences, Rush University Medical Center, Chicago, IL USA.</nlm:affiliation></affiliation></author><author><name sortKey="Buvanendran, Asokumar" sort="Buvanendran, Asokumar" uniqKey="Buvanendran A" first="Asokumar" last="Buvanendran">Asokumar Buvanendran</name><affiliation><nlm:affiliation>Department of Behavioral Sciences, Rush University Medical Center, Chicago, IL USA.</nlm:affiliation></affiliation></author><author><name sortKey="Chont, Melissa" sort="Chont, Melissa" uniqKey="Chont M" first="Melissa" last="Chont">Melissa Chont</name><affiliation><nlm:affiliation>Department of Anesthesiology, Vanderbilt University School of Medicine, Vanderbilt, TN, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Gupta, Rajnish K" sort="Gupta, Rajnish K" uniqKey="Gupta R" first="Rajnish K" last="Gupta">Rajnish K. Gupta</name><affiliation><nlm:affiliation>Department of Anesthesiology, Vanderbilt University School of Medicine, Vanderbilt, TN, USA.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Pain</title><idno type="eISSN">1872-6623</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Administration, Intravenous (MeSH)</term><term>Adult (MeSH)</term><term>Analgesics, Opioid (administration & dosage)</term><term>Catastrophization (chemically induced)</term><term>Catastrophization (psychology)</term><term>Chronic Pain (drug therapy)</term><term>Chronic Pain (psychology)</term><term>Cross-Over Studies (MeSH)</term><term>Double-Blind Method (MeSH)</term><term>Female (MeSH)</term><term>Humans (MeSH)</term><term>Low Back Pain (drug therapy)</term><term>Low Back Pain (psychology)</term><term>Male (MeSH)</term><term>Middle Aged (MeSH)</term><term>Mood Disorders (chemically induced)</term><term>Morphine (administration & dosage)</term><term>Naloxone (administration & dosage)</term><term>Narcotic Antagonists (administration & dosage)</term><term>Pain Measurement (MeSH)</term><term>Pain Threshold (drug effects)</term><term>Pain Threshold (physiology)</term><term>Psychiatric Status Rating Scales (MeSH)</term><term>Self Report (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Analgesics, Opioid</term><term>Morphine</term><term>Naloxone</term><term>Narcotic Antagonists</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Catastrophization</term><term>Mood Disorders</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Pain Threshold</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Chronic Pain</term><term>Low Back Pain</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Pain Threshold</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Catastrophization</term><term>Chronic Pain</term><term>Low Back Pain</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Administration, Intravenous</term><term>Adult</term><term>Cross-Over Studies</term><term>Double-Blind Method</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Pain Measurement</term><term>Psychiatric Status Rating Scales</term><term>Self Report</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Use of opioid analgesics for management of chronic nonmalignant pain has become common, yet there are presently no well-validated predictors of optimal opioid analgesic efficacy. We examined whether psychosocial factors (eg, depressive symptoms) predicted changes in spontaneous low back pain after administration of opioid analgesics, and whether endogenous opioid (EO) function mediated these relationships. Participants with chronic low back pain but who were not chronic opioid users (N = 89) underwent assessment of low back pain intensity pre- and post-drug in 3 (counterbalanced) conditions: (1) placebo, (2) intravenous naloxone, and (3) intravenous morphine. Comparison of placebo condition changes in back pain intensity to those under naloxone and morphine provided indexes of EO function and opioid analgesic responses, respectively. Results showed that (1) most psychosocial variables were related significantly and positively to morphine analgesic responses for low back pain, (2) depressive symptoms, trait anxiety, pain catastrophizing, and pain disability were related negatively to EO function, and (3) EO function was related negatively to morphine analgesic responses for low back pain. Bootstrapped mediation analyses showed that links between morphine analgesic responses and depressive symptoms, trait anxiety, pain catastrophizing, and perceived disability were partially mediated by EO function. Results suggest that psychosocial factors predict elevated analgesic responses to opioid-based medications, and may serve as markers to identify individuals who benefit most from opioid therapy. Results also suggest that people with greater depressive symptoms, trait anxiety, pain catastrophizing, and perceived disability may have deficits in EO function, which may predict enhanced response to opioid analgesics.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27898491</PMID><DateCompleted><Year>2017</Year><Month>11</Month><Day>21</Day></DateCompleted><DateRevised><Year>2021</Year><Month>01</Month><Day>12</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1872-6623</ISSN><JournalIssue CitedMedium="Internet"><Volume>158</Volume><Issue>3</Issue><PubDate><Year>2017</Year><Month>03</Month></PubDate></JournalIssue><Title>Pain</Title><ISOAbbreviation>Pain</ISOAbbreviation></Journal><ArticleTitle>Psychosocial factors predict opioid analgesia through endogenous opioid function.</ArticleTitle><Pagination><MedlinePgn>391-399</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1097/j.pain.0000000000000768</ELocationID><Abstract><AbstractText>Use of opioid analgesics for management of chronic nonmalignant pain has become common, yet there are presently no well-validated predictors of optimal opioid analgesic efficacy. We examined whether psychosocial factors (eg, depressive symptoms) predicted changes in spontaneous low back pain after administration of opioid analgesics, and whether endogenous opioid (EO) function mediated these relationships. Participants with chronic low back pain but who were not chronic opioid users (N = 89) underwent assessment of low back pain intensity pre- and post-drug in 3 (counterbalanced) conditions: (1) placebo, (2) intravenous naloxone, and (3) intravenous morphine. Comparison of placebo condition changes in back pain intensity to those under naloxone and morphine provided indexes of EO function and opioid analgesic responses, respectively. Results showed that (1) most psychosocial variables were related significantly and positively to morphine analgesic responses for low back pain, (2) depressive symptoms, trait anxiety, pain catastrophizing, and pain disability were related negatively to EO function, and (3) EO function was related negatively to morphine analgesic responses for low back pain. Bootstrapped mediation analyses showed that links between morphine analgesic responses and depressive symptoms, trait anxiety, pain catastrophizing, and perceived disability were partially mediated by EO function. Results suggest that psychosocial factors predict elevated analgesic responses to opioid-based medications, and may serve as markers to identify individuals who benefit most from opioid therapy. Results also suggest that people with greater depressive symptoms, trait anxiety, pain catastrophizing, and perceived disability may have deficits in EO function, which may predict enhanced response to opioid analgesics.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Burns</LastName><ForeName>John W</ForeName><Initials>JW</Initials><AffiliationInfo><Affiliation>Department of Behavioral Sciences, Rush University Medical Center, Chicago, IL USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bruehl</LastName><ForeName>Stephen</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Vanderbilt University School of Medicine, Vanderbilt, TN, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>France</LastName><ForeName>Christopher R</ForeName><Initials>CR</Initials><AffiliationInfo><Affiliation>Department of Psychology, Ohio University, Athens, OH, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schuster</LastName><ForeName>Erik</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Behavioral Sciences, Rush University Medical Center, Chicago, IL USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Orlowska</LastName><ForeName>Daria</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Behavioral Sciences, Rush University Medical Center, Chicago, IL USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Buvanendran</LastName><ForeName>Asokumar</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Behavioral Sciences, Rush University Medical Center, Chicago, IL USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chont</LastName><ForeName>Melissa</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Vanderbilt University School of Medicine, Vanderbilt, TN, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gupta</LastName><ForeName>Rajnish K</ForeName><Initials>RK</Initials><AffiliationInfo><Affiliation>Department of Anesthesiology, Vanderbilt University School of Medicine, Vanderbilt, TN, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 DA031726</GrantID><Acronym>DA</Acronym><Agency>NIDA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DA037891</GrantID><Acronym>DA</Acronym><Agency>NIDA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016448">Multicenter Study</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Pain</MedlineTA><NlmUniqueID>7508686</NlmUniqueID><ISSNLinking>0304-3959</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000701">Analgesics, Opioid</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009292">Narcotic Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>36B82AMQ7N</RegistryNumber><NameOfSubstance UI="D009270">Naloxone</NameOfSubstance></Chemical><Chemical><RegistryNumber>76I7G6D29C</RegistryNumber><NameOfSubstance UI="D009020">Morphine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D061605" MajorTopicYN="N">Administration, Intravenous</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000701" MajorTopicYN="N">Analgesics, Opioid</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058443" MajorTopicYN="N">Catastrophization</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="Y">chemically induced</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059350" MajorTopicYN="N">Chronic Pain</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018592" MajorTopicYN="N">Cross-Over Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004311" MajorTopicYN="N">Double-Blind Method</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017116" MajorTopicYN="N">Low Back Pain</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000523" MajorTopicYN="Y">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019964" MajorTopicYN="N">Mood Disorders</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="Y">chemically induced</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009020" MajorTopicYN="N">Morphine</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009270" MajorTopicYN="N">Naloxone</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009292" MajorTopicYN="N">Narcotic Antagonists</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010147" MajorTopicYN="N">Pain Measurement</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017288" MajorTopicYN="N">Pain Threshold</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011569" MajorTopicYN="N">Psychiatric Status Rating Scales</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D057566" MajorTopicYN="N">Self Report</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>11</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>11</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>11</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27898491</ArticleId><ArticleId IdType="doi">10.1097/j.pain.0000000000000768</ArticleId><ArticleId IdType="pmc">PMC7176103</ArticleId><ArticleId IdType="mid">NIHMS829463</ArticleId><ArticleId IdType="pii">00006396-201703000-00006</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Arteta J, Cobos B, Hu Y, Jordan K, Howard K. Evaluation of how depression and anxiety mediate the relationship between pain catastrophizing and prescription opioid misuse in a chronic pain population. Pain Med 2016;17:295–303.</Citation></Reference><Reference><Citation>Baron RM, Kenny DA. The moderator-mediator variable distinction in social psychological research: conceptual, strategic, and statistical considerations. J Personal Soc Psychol 1986;51:1173–82.</Citation></Reference><Reference><Citation>Beck AT, Ward CH, Mendelson M, Mock JE, Erbough JK. An inventory for measuring depression. Arch Gen Psychiatr 1961;4:561–71.</Citation></Reference><Reference><Citation>Berkowitz BA, Ngai SH, Hempstead J, Spector S. Disposition of naloxone: use of a new radioimmunoassay. J Pharmacol Exp Ther 1975;195:499–504.</Citation></Reference><Reference><Citation>Bruehl S, Burns JW, Chung OY, Quartana P. Anger management style and emotional reactivity to noxious stimuli among chronic pain patients and healthy controls: the role of endogenous opioids. Health Psychol 2008;27:204–14.</Citation></Reference><Reference><Citation>Bruehl S, Burns JW, Chung OY, Ward P, Johnson B. Anger and pain sensitivity in chronic low back pain patients and pain-free controls: the role of endogenous opioids. PAIN 2002;99:223–33.</Citation></Reference><Reference><Citation>Bruehl S, Burns JW, Gupta R, Buvanendran A, Chont M, Kinner E, Schuster E, Passik S, France CR. Endogenous opioid function mediates the association between laboratory evoked pain sensitivity and morphine analgesic responses. PAIN 2013;154:1856–64.</Citation></Reference><Reference><Citation>Bruehl S, Burns JW, Gupta R, Buvanendran A, Chont M, Schuster EM, France CR. Endogenous opioid inhibition of chronic low back pain influences degree of back pain relief following morphine administration. Reg Anesth Pain Med 2014;39:120–5.</Citation></Reference><Reference><Citation>Bruehl S, Burns JW, Passik SD, Gupta R, Buvanendran A, Chont M, Schuster E, Orlowska D, France CR. The contribution of differential opioid responsiveness to identification of opioid risk in chronic pain patients. J Pain 2015;16:666–75.</Citation></Reference><Reference><Citation>Bruehl S, Chung OY, Burns JW. Trait anger and blood pressure recovery following acute pain: evidence for opioid-mediated effects. Int J Behav Med 2006;13:138–46.</Citation></Reference><Reference><Citation>Bruehl S, Chung OY, Burns JW, Biridepalli S. The association between anger expression and chronic pain intensity: evidence for partial mediation by endogenous opioid dysfunction. PAIN 2003;106:317–24.</Citation></Reference><Reference><Citation>Bruehl S, Chung OY, Burns JW, Diedrich L. Trait anger expressiveness and pain-induced beta-endorphin release: support for the opioid dysfunction hypothesis. PAIN 2007;130:208–15.</Citation></Reference><Reference><Citation>Burns JW, Bruehl S, Chung OY, Magid E, Chont M, Goodlad JK, Gilliam W, Matsuura J, Somar K. Endogenous opioids may buffer effects of anger arousal on sensitivity to subsequent pain. PAIN 2009;146:276–82.</Citation></Reference><Reference><Citation>Caudill-Slosberg MA, Schwartz LM, Woloshin S. Office visits and analgesic prescriptions for musculoskeletal pain in US: 1980 vs 2000. PAIN 2004;109:514–19.</Citation></Reference><Reference><Citation>Chou R, Fanciullo GJ, Fine PG, Miaskowski C, Passik SD, Portenoy RK. Opioids for chronic noncancer pain: prediction and identification of aberrant drug-related behaviors: a review of the evidence for an American Pain Society and American Academy of Pain Medicine clinical practice guidelines. J Pain 2009;10:131–46.</Citation></Reference><Reference><Citation>De Cosmo G, Congedo E, Lai C, Primieri P, Dottarelli A, Aceto P. Preoperative psychologic and demographic predictors of pain perception and tramadol consumption using intravenous patient controlled analgesia. Clin J Pain 2008;24:399–405.</Citation></Reference><Reference><Citation>Dunn KM, Saunders KW, Rutter CM, Banta-Green CJ, Merrill JO, Sullivan MD, Weisner CM, Silverberg MJ, Campbell CI, Psaty BM, Von Korff M. Opioid prescriptions for chronic pain and overdose: a cohort study. Ann Intern Med 2010;152:85–92.</Citation></Reference><Reference><Citation>Fillingim RB, Hastie BA, Ness TJ, Glover TL, Campbell CM, Staud R. Sex-related psychological predictors of baseline pain perception and analgesic responses to pentazocine. Biol Psychol 2005;69:97–112.</Citation></Reference><Reference><Citation>Fillingim RB, Ness TJ, Glover TL, Campbell CM, Hastie BA, Price DD, Staud R. Morphine responses and experimental pain: sex differences in side effects and cardiovascular responses but not analgesia. J Pain 2005;6:116–24.</Citation></Reference><Reference><Citation>Geha H, Nimeskern N, Beziat JL. Patient-controlled analgesia in orthognathic surgery: evaluation of the relationship to anxiety and anxiolytics. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2009;108:e33–6.</Citation></Reference><Reference><Citation>Harris RE, Zubieta JK, Scott DJ, Napadow V, Gracely RH, Clauw DJ. Traditional Chinese acupuncture and placebo (sham) acupuncture are differentiated by their effects on mu-opioid receptors (MORs). Neuroimage 2009;47:1077–85.</Citation></Reference><Reference><Citation>Kennedy SE, Koeppe RA, Young EA, Zubieta JK. Dysregulation of endogenous opioid emotion regulation circuitry in major depression in women. Arch Gen Psychiatry 2006;63:1199–208.</Citation></Reference><Reference><Citation>Kidner CL, Mayer TG, Gatchel RJ. Higher opioid doses predict poorer functional outcome in patients with chronic disabling occupational musculoskeletal disorders. J Bone Joint Surg Am 2009;91:919–27.</Citation></Reference><Reference><Citation>Koltyn KF. Analgesia following exercise: a review. Sports Med 2000;29:85–98.</Citation></Reference><Reference><Citation>Lewis J, Mansour A, Khachaturian H, Watson SJ, Akil H. Opioids and pain regulation. Pain Headache 1987;9:129–59.</Citation></Reference><Reference><Citation>Martin WR. Drugs five years later: naloxone. Ann Intern Med 1976;85:765–8.</Citation></Reference><Reference><Citation>McCubbin JA, Cheung R, Montgomery TB, Bulbulian R, Wilson JF. Aerobic fitness and opioidergic inhibition of cardiovascular stress reactivity. Psychophys 1992;29:687–97.</Citation></Reference><Reference><Citation>McCubbin JA, Wilson JF, Bruehl S, Ibarra P, Carlson CR, Norton JA, Colclough GW. Relaxation training and opioid inhibition of blood pressure response to stress. J Consult Clin Psychol 1996;64:593–601.</Citation></Reference><Reference><Citation>Melzack R. The short form of the McGill pain questionnaire. PAIN 1987;30:191–7.</Citation></Reference><Reference><Citation>Millan MJ. Descending control of pain. Prog Neurobiol 2002;66:355–474.</Citation></Reference><Reference><Citation>Okie S. A flood of opioids, a rising tide of deaths. N Engl J Med 2010;363:1981–5.</Citation></Reference><Reference><Citation>Osman A, Barrios FX, Kopper BA, Hauptmann W, Jones J, O'Neill E. Factor structure, reliability, and validity of the pain catastrophizing scale. J Behav Med 1997;20:589–605.</Citation></Reference><Reference><Citation>Perry F, Parker RK, White PF. Clifford PA Role of psychological factors in postoperative pain control and recovery with patient-controlled analgesia. Clin J Pain 1994;10:57–63.</Citation></Reference><Reference><Citation>Petraschka M, Li S, Gilbert TL, Westenbroek RE, Bruchas MR, Schreiber S, Lowe J, Low MJ, Pintar JE, Chavkin C. The absence of endogenous beta-endorphin selectively blocks phosphorylation and desensitization of mu opioid receptors following partial sciatic nerve ligation. Neuroscience 2007;146:1795–807.</Citation></Reference><Reference><Citation>Preacher KJ, Hayes AF. SPSS and SAS procedures for estimating indirect effects in simple mediation models. Behav Res Methods Instrum Comput 2004;36:717–31.</Citation></Reference><Reference><Citation>Raehal KM, Bohn LM. The role of beta-arrest in 2 in the severity of antinociceptive tolerance and physical dependence induced by different opioid pain therapeutics. Neuropharm 2011;60:58–65.</Citation></Reference><Reference><Citation>Spielberger CD, Gorsuch RL, Lushene RE. Manual for the State-Trait Anxiety Inventory. Palo Alto: Consulting Psychologists Press, 1970.</Citation></Reference><Reference><Citation>Spielberger CD, Jacobs G, Russell S, Crane R. Assessment of anger: The State-Trait Anger Scale. In: Butcher JN, Spielberger CD, editors. Advances in personality assessment. Vol. 2. Hillsdale: LEA, 1983. p. 161–89.</Citation></Reference><Reference><Citation>Sullivan MJL, Bishop SR, Pivik J. The pain catastrophizing scale: development and validation. Psychol Assess 1995;7:524–32.</Citation></Reference><Reference><Citation>Tait RC, Chibnall JT, Krause S.The Pain Disability Index: psychometric properties. PAIN 1990;40:171–82.</Citation></Reference><Reference><Citation>Tseng LF, Lin JJ, Collins KA. Partial antinociceptive cross-tolerance to intracerebroventricular [beta]-endorphin in mice tolerant to systemic morphine. Euro J Pharmac 1993;241:63–70.</Citation></Reference><Reference><Citation>Turk DC, Swanson KS, Gatchel RJ. Predicting opioid misuse by chronic pain patients: a systematic review and literature synthesis. Clin J Pain 2008;24:497–508.</Citation></Reference><Reference><Citation>Wardlaw SL, Kim J, Sobieszczyk S. Effect of morphine on proopiomelanocortin gene expression and peptide levels in the hypothalamus. Mol Brain Res 1996;41:140–7.</Citation></Reference><Reference><Citation>Wasan AD, Davar G, Jamison R. The association between negative affect and opioid analgesia in patients with discogenic low back pain. PAIN 2005;117:450–61.</Citation></Reference><Reference><Citation>Watson D, Clark LA, Tellegen A. Development and validation of brief measures of positive and negative affect: The PANAS scales. J Personal Soc Psychol 1988;54:1063–70.</Citation></Reference></ReferenceList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/AutomedicationFrancoV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000C74 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 000C74 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= AutomedicationFrancoV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= pubmed:27898491
|texte= Psychosocial factors predict opioid analgesia through endogenous opioid function.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Corpus/RBID.i -Sk "pubmed:27898491" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd \
| NlmPubMed2Wicri -a AutomedicationFrancoV1
| This area was generated with Dilib version V0.6.38. |  |