Dysfunctional stress responses in chronic pain.
Identifieur interne : 001916 ( PubMed/Corpus ); précédent : 001915; suivant : 001917Dysfunctional stress responses in chronic pain.
Auteurs : Alain Woda ; Pascale Picard ; Frédéric DutheilSource :
- Psychoneuroendocrinology [ 1873-3360 ] ; 2016.
English descriptors
- KwdEn :
- Chronic Pain (metabolism), Chronic Pain (physiopathology), Cushing Syndrome (metabolism), Cytokines (immunology), Cytokines (metabolism), Dehydroepiandrosterone (metabolism), Dehydroepiandrosterone Sulfate (metabolism), Humans, Hypothalamo-Hypophyseal System (metabolism), Pituitary-Adrenal System (metabolism), Progesterone, Th1 Cells (immunology), Th2 Cells (immunology).
- MESH :
- chemical , immunology : Cytokines.
- immunology : Th1 Cells, Th2 Cells.
- metabolism : Chronic Pain, Cushing Syndrome, Cytokines, Dehydroepiandrosterone, Dehydroepiandrosterone Sulfate, Hypothalamo-Hypophyseal System, Pituitary-Adrenal System.
- physiopathology : Chronic Pain.
- Humans, Progesterone.
Abstract
Many dysfunctional and chronic pain conditions overlap. This review describes the different modes of chronic deregulation of the adaptive response to stress which may be a common factor for these conditions. Several types of dysfunction can be identified within the hypothalamo-pituitary-adrenal axis: basal hypercortisolism, hyper-reactivity, basal hypocortisolism and hypo-reactivity. Neuroactive steroid synthesis is another component of the adaptive response to stress. Dehydroepiandrosterone (DHEA) and its sulfated form DHEA-S, and progesterone and its derivatives are synthetized in cutaneous, nervous, and adipose cells. They are neuroactive factors that act locally. They may have a role in the localization of the symptoms and their levels can vary both in the central nervous system and in the periphery. Persistent changes in neuroactive steroid levels or precursors can induce localized neurodegeneration. The autonomic nervous system is another component of the stress response. Its dysfunction in chronic stress responses can be expressed by decreased basal parasympathethic activity, increased basal sympathetic activity or sympathetic hyporeactivity to a stressful stimulus. The immune and genetic systems also participate. The helper-T cells Th1 secrete pro-inflammatory cytokines such as IL-1-β, IL-2, IL-6, IL-8, IL-12, IFN-γ, and TNF-α, whereas Th2 secrete anti-inflammatory cytokines: IL-4, IL-10, IGF-10, IL-13. Chronic deregulation of the Th1/Th2 balance can occur in favor of anti- or pro-inflammatory direction, locally or systemically. Individual vulnerability to stress can be due to environmental factors but can also be genetically influenced. Genetic polymorphisms and epigenetics are the main keys to understanding the influence of genetics on the response of individuals to constraints.
DOI: 10.1016/j.psyneuen.2016.05.017
PubMed: 27262345
Links to Exploration step
pubmed:27262345Le document en format XML
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Electronic address: frederic.dutheil@acu.edu.au.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27262345</idno><idno type="pmid">27262345</idno><idno type="doi">10.1016/j.psyneuen.2016.05.017</idno><idno type="wicri:Area/PubMed/Corpus">001916</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001916</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Dysfunctional stress responses in chronic pain.</title><author><name sortKey="Woda, Alain" sort="Woda, Alain" uniqKey="Woda A" first="Alain" last="Woda">Alain Woda</name><affiliation><nlm:affiliation>Dental faculty, EA 3847, CROC, 11 Boulevard Charles-de-Gaulle, Clermont-Ferrand, France; University Hospital of Clermont-Ferrand (CHU), Odontology department, Clermont-Ferrand, France.</nlm:affiliation></affiliation></author><author><name sortKey="Picard, Pascale" sort="Picard, Pascale" uniqKey="Picard P" first="Pascale" last="Picard">Pascale Picard</name><affiliation><nlm:affiliation>Pain center, University Hospital of Clermont-Ferrand (CHU), Clermont-Ferrand, France.</nlm:affiliation></affiliation></author><author><name sortKey="Dutheil, Frederic" sort="Dutheil, Frederic" uniqKey="Dutheil F" first="Frédéric" last="Dutheil">Frédéric Dutheil</name><affiliation><nlm:affiliation>Preventive and Occupational Medicine, University Hospital of Clermont-Ferrand (CHU), Clermont-Ferrand, France; University Clermont Auvergne, Laboratory of Metabolic Adaptations to Exercise in Physiological and Pathological conditions (AME2P, EA3533), Clermont-Ferrand, France; Australian Catholic University, Faculty of Health, Melbourne, Victoria, Australia; CNRS, UMR 6024, Physiological and Psychosocial Stress, LAPSCO, University Clermont Auvergne, Clermont-Ferrand, France. Electronic address: frederic.dutheil@acu.edu.au.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Psychoneuroendocrinology</title><idno type="eISSN">1873-3360</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Chronic Pain (metabolism)</term><term>Chronic Pain (physiopathology)</term><term>Cushing Syndrome (metabolism)</term><term>Cytokines (immunology)</term><term>Cytokines (metabolism)</term><term>Dehydroepiandrosterone (metabolism)</term><term>Dehydroepiandrosterone Sulfate (metabolism)</term><term>Humans</term><term>Hypothalamo-Hypophyseal System (metabolism)</term><term>Pituitary-Adrenal System (metabolism)</term><term>Progesterone</term><term>Th1 Cells (immunology)</term><term>Th2 Cells (immunology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Th1 Cells</term><term>Th2 Cells</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Chronic Pain</term><term>Cushing Syndrome</term><term>Cytokines</term><term>Dehydroepiandrosterone</term><term>Dehydroepiandrosterone Sulfate</term><term>Hypothalamo-Hypophyseal System</term><term>Pituitary-Adrenal System</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Chronic Pain</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Progesterone</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Many dysfunctional and chronic pain conditions overlap. This review describes the different modes of chronic deregulation of the adaptive response to stress which may be a common factor for these conditions. Several types of dysfunction can be identified within the hypothalamo-pituitary-adrenal axis: basal hypercortisolism, hyper-reactivity, basal hypocortisolism and hypo-reactivity. Neuroactive steroid synthesis is another component of the adaptive response to stress. Dehydroepiandrosterone (DHEA) and its sulfated form DHEA-S, and progesterone and its derivatives are synthetized in cutaneous, nervous, and adipose cells. They are neuroactive factors that act locally. They may have a role in the localization of the symptoms and their levels can vary both in the central nervous system and in the periphery. Persistent changes in neuroactive steroid levels or precursors can induce localized neurodegeneration. The autonomic nervous system is another component of the stress response. Its dysfunction in chronic stress responses can be expressed by decreased basal parasympathethic activity, increased basal sympathetic activity or sympathetic hyporeactivity to a stressful stimulus. The immune and genetic systems also participate. The helper-T cells Th1 secrete pro-inflammatory cytokines such as IL-1-β, IL-2, IL-6, IL-8, IL-12, IFN-γ, and TNF-α, whereas Th2 secrete anti-inflammatory cytokines: IL-4, IL-10, IGF-10, IL-13. Chronic deregulation of the Th1/Th2 balance can occur in favor of anti- or pro-inflammatory direction, locally or systemically. Individual vulnerability to stress can be due to environmental factors but can also be genetically influenced. Genetic polymorphisms and epigenetics are the main keys to understanding the influence of genetics on the response of individuals to constraints.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27262345</PMID><DateCreated><Year>2016</Year><Month>07</Month><Day>19</Day></DateCreated><DateCompleted><Year>2017</Year><Month>09</Month><Day>18</Day></DateCompleted><DateRevised><Year>2017</Year><Month>09</Month><Day>18</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-3360</ISSN><JournalIssue CitedMedium="Internet"><Volume>71</Volume><PubDate><Year>2016</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Psychoneuroendocrinology</Title><ISOAbbreviation>Psychoneuroendocrinology</ISOAbbreviation></Journal><ArticleTitle>Dysfunctional stress responses in chronic pain.</ArticleTitle><Pagination><MedlinePgn>127-35</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.psyneuen.2016.05.017</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0306-4530(16)30148-2</ELocationID><Abstract><AbstractText>Many dysfunctional and chronic pain conditions overlap. This review describes the different modes of chronic deregulation of the adaptive response to stress which may be a common factor for these conditions. Several types of dysfunction can be identified within the hypothalamo-pituitary-adrenal axis: basal hypercortisolism, hyper-reactivity, basal hypocortisolism and hypo-reactivity. Neuroactive steroid synthesis is another component of the adaptive response to stress. Dehydroepiandrosterone (DHEA) and its sulfated form DHEA-S, and progesterone and its derivatives are synthetized in cutaneous, nervous, and adipose cells. They are neuroactive factors that act locally. They may have a role in the localization of the symptoms and their levels can vary both in the central nervous system and in the periphery. Persistent changes in neuroactive steroid levels or precursors can induce localized neurodegeneration. The autonomic nervous system is another component of the stress response. Its dysfunction in chronic stress responses can be expressed by decreased basal parasympathethic activity, increased basal sympathetic activity or sympathetic hyporeactivity to a stressful stimulus. The immune and genetic systems also participate. The helper-T cells Th1 secrete pro-inflammatory cytokines such as IL-1-β, IL-2, IL-6, IL-8, IL-12, IFN-γ, and TNF-α, whereas Th2 secrete anti-inflammatory cytokines: IL-4, IL-10, IGF-10, IL-13. Chronic deregulation of the Th1/Th2 balance can occur in favor of anti- or pro-inflammatory direction, locally or systemically. Individual vulnerability to stress can be due to environmental factors but can also be genetically influenced. Genetic polymorphisms and epigenetics are the main keys to understanding the influence of genetics on the response of individuals to constraints.</AbstractText><CopyrightInformation>Copyright © 2016 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Woda</LastName><ForeName>Alain</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Dental faculty, EA 3847, CROC, 11 Boulevard Charles-de-Gaulle, Clermont-Ferrand, France; University Hospital of Clermont-Ferrand (CHU), Odontology department, Clermont-Ferrand, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Picard</LastName><ForeName>Pascale</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Pain center, University Hospital of Clermont-Ferrand (CHU), Clermont-Ferrand, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dutheil</LastName><ForeName>Frédéric</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Preventive and Occupational Medicine, University Hospital of Clermont-Ferrand (CHU), Clermont-Ferrand, France; University Clermont Auvergne, Laboratory of Metabolic Adaptations to Exercise in Physiological and Pathological conditions (AME2P, EA3533), Clermont-Ferrand, France; Australian Catholic University, Faculty of Health, Melbourne, Victoria, Australia; CNRS, UMR 6024, Physiological and Psychosocial Stress, LAPSCO, University Clermont Auvergne, Clermont-Ferrand, France. Electronic address: frederic.dutheil@acu.edu.au.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>05</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Psychoneuroendocrinology</MedlineTA><NlmUniqueID>7612148</NlmUniqueID><ISSNLinking>0306-4530</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>459AG36T1B</RegistryNumber><NameOfSubstance UI="D003687">Dehydroepiandrosterone</NameOfSubstance></Chemical><Chemical><RegistryNumber>4G7DS2Q64Y</RegistryNumber><NameOfSubstance UI="D011374">Progesterone</NameOfSubstance></Chemical><Chemical><RegistryNumber>57B09Q7FJR</RegistryNumber><NameOfSubstance UI="D019314">Dehydroepiandrosterone Sulfate</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D059350" MajorTopicYN="N">Chronic Pain</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003480" MajorTopicYN="N">Cushing Syndrome</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003687" MajorTopicYN="N">Dehydroepiandrosterone</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019314" MajorTopicYN="N">Dehydroepiandrosterone Sulfate</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007030" MajorTopicYN="N">Hypothalamo-Hypophyseal System</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010913" MajorTopicYN="N">Pituitary-Adrenal System</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011374" MajorTopicYN="N">Progesterone</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018417" MajorTopicYN="N">Th1 Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018418" MajorTopicYN="N">Th2 Cells</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Acute</Keyword><Keyword MajorTopicYN="N">Autonomic nervous system</Keyword><Keyword MajorTopicYN="N">Chronic</Keyword><Keyword MajorTopicYN="N">Disease</Keyword><Keyword MajorTopicYN="N">Environment</Keyword><Keyword MajorTopicYN="N">Physiopathology</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>01</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>04</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>05</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>6</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>6</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>9</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27262345</ArticleId><ArticleId IdType="pii">S0306-4530(16)30148-2</ArticleId><ArticleId IdType="doi">10.1016/j.psyneuen.2016.05.017</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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