Increased basal mechanical pain sensitivity but decreased perceptual wind-up in a human model of relative hypocortisolism.
Identifieur interne : 000533 ( PubMed/Curation ); précédent : 000532; suivant : 000534Increased basal mechanical pain sensitivity but decreased perceptual wind-up in a human model of relative hypocortisolism.
Auteurs : Linn K. Kuehl [Allemagne] ; Gilles P. Michaux ; Steffen Richter ; Hartmut Sch Chinger ; Fernand AntonSource :
- Pain [ 1872-6623 ] ; 2010.
English descriptors
- KwdEn :
- Adult, Chronic Disease, Cross-Over Studies, Endocrine System Diseases (chemically induced), Endocrine System Diseases (complications), Endocrine System Diseases (physiopathology), Humans, Hydrocortisone (blood), Hydrocortisone (deficiency), Hydrocortisone (secretion), Hyperalgesia (blood), Hyperalgesia (etiology), Hyperalgesia (physiopathology), Hypothalamo-Hypophyseal System (metabolism), Hypothalamo-Hypophyseal System (physiopathology), Hypothalamo-Hypophyseal System (secretion), Male, Pain (blood), Pain (etiology), Pain (physiopathology), Pain Measurement (methods), Pain Threshold (physiology), Perception (physiology), Pituitary-Adrenal System (metabolism), Pituitary-Adrenal System (physiopathology), Pituitary-Adrenal System (secretion), Young Adult.
- MESH :
- chemical , blood : Hydrocortisone.
- blood : Hyperalgesia, Pain.
- chemically induced : Endocrine System Diseases.
- complications : Endocrine System Diseases.
- chemical , deficiency : Hydrocortisone.
- etiology : Hyperalgesia, Pain.
- metabolism : Hypothalamo-Hypophyseal System, Pituitary-Adrenal System.
- methods : Pain Measurement.
- physiology : Pain Threshold, Perception.
- physiopathology : Endocrine System Diseases, Hyperalgesia, Hypothalamo-Hypophyseal System, Pain, Pituitary-Adrenal System.
- chemical , secretion : Hydrocortisone, Hypothalamo-Hypophyseal System, Pituitary-Adrenal System.
- Adult, Chronic Disease, Cross-Over Studies, Humans, Male, Young Adult.
Abstract
Clinical data have accumulated showing that relative hypocortisolism, which may be regarded as a neuroendocrinological correlate of chronic stress, may be a characteristic of some functional pain syndromes. However, it has not been clarified yet whether deregulations of the hypothalamus-pituitary-adrenal (HPA) axis may directly alter pain perception and thus be causally involved in the pathophysiology of these disorders. To test this hypothesis, we performed a randomized placebo-controlled crossover trial in N=20 healthy drug-free volunteers (median age 24yrs) and analyzed the effects of metyrapone-induced hypocortisolism on quantitatively assessed basal mechanical pain sensitivity (1.5-13m/s impact stimuli), perceptual wind-up (9m/s impact stimuli at 1Hz) and temporal summation of pain elicited by inter-digital web pinching (IWP; 10N pressure stimuli for 2min). Experimentally induced hypocortisolism significantly decreased pain detection thresholds and augmented temporal summation of IWP-induced pain (p<.05). The latter effect was dependent on the relative reduction in cortisol levels, and seemed to rely on a potentiated sensitization and not merely on the observed changes in basal pain sensitivity. Perceptual wind-up by contrast was reduced when cortisol synthesis was blocked (p<.05). This result is reminiscent of findings from animal studies showing a reversal of NMDA receptor activation by glucocorticoid receptor antagonists in neuropathic pain models. Our results speak in favor of a potential causal role of HPA axis alterations in pain chronicity.
DOI: 10.1016/j.pain.2010.03.026
PubMed: 20381248
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Michaux</name></author><author><name sortKey="Richter, Steffen" sort="Richter, Steffen" uniqKey="Richter S" first="Steffen" last="Richter">Steffen Richter</name></author><author><name sortKey="Sch Chinger, Hartmut" sort="Sch Chinger, Hartmut" uniqKey="Sch Chinger H" first="Hartmut" last="Sch Chinger">Hartmut Sch Chinger</name></author><author><name sortKey="Anton, Fernand" sort="Anton, Fernand" uniqKey="Anton F" first="Fernand" last="Anton">Fernand Anton</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="RBID">pubmed:20381248</idno><idno type="pmid">20381248</idno><idno type="doi">10.1016/j.pain.2010.03.026</idno><idno type="wicri:Area/PubMed/Corpus">000533</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000533</idno><idno type="wicri:Area/PubMed/Curation">000533</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000533</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Increased basal mechanical pain sensitivity but decreased perceptual wind-up in a human model of relative hypocortisolism.</title><author><name sortKey="Kuehl, Linn K" sort="Kuehl, Linn K" uniqKey="Kuehl L" first="Linn K" last="Kuehl">Linn K. Kuehl</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Psychobiology, Department of Clinical Physiology, University of Trier, Johanniterufer 15, Trier, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institute of Psychobiology, Department of Clinical Physiology, University of Trier, Johanniterufer 15, Trier</wicri:regionArea></affiliation></author><author><name sortKey="Michaux, Gilles P" sort="Michaux, Gilles P" uniqKey="Michaux G" first="Gilles P" last="Michaux">Gilles P. Michaux</name></author><author><name sortKey="Richter, Steffen" sort="Richter, Steffen" uniqKey="Richter S" first="Steffen" last="Richter">Steffen Richter</name></author><author><name sortKey="Sch Chinger, Hartmut" sort="Sch Chinger, Hartmut" uniqKey="Sch Chinger H" first="Hartmut" last="Sch Chinger">Hartmut Sch Chinger</name></author><author><name sortKey="Anton, Fernand" sort="Anton, Fernand" uniqKey="Anton F" first="Fernand" last="Anton">Fernand Anton</name></author></analytic><series><title level="j">Pain</title><idno type="eISSN">1872-6623</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Chronic Disease</term><term>Cross-Over Studies</term><term>Endocrine System Diseases (chemically induced)</term><term>Endocrine System Diseases (complications)</term><term>Endocrine System Diseases (physiopathology)</term><term>Humans</term><term>Hydrocortisone (blood)</term><term>Hydrocortisone (deficiency)</term><term>Hydrocortisone (secretion)</term><term>Hyperalgesia (blood)</term><term>Hyperalgesia (etiology)</term><term>Hyperalgesia (physiopathology)</term><term>Hypothalamo-Hypophyseal System (metabolism)</term><term>Hypothalamo-Hypophyseal System (physiopathology)</term><term>Hypothalamo-Hypophyseal System (secretion)</term><term>Male</term><term>Pain (blood)</term><term>Pain (etiology)</term><term>Pain (physiopathology)</term><term>Pain Measurement (methods)</term><term>Pain Threshold (physiology)</term><term>Perception (physiology)</term><term>Pituitary-Adrenal System (metabolism)</term><term>Pituitary-Adrenal System (physiopathology)</term><term>Pituitary-Adrenal System (secretion)</term><term>Young Adult</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Hydrocortisone</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Hyperalgesia</term><term>Pain</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Endocrine System Diseases</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Endocrine System Diseases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Hydrocortisone</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Hyperalgesia</term><term>Pain</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Hypothalamo-Hypophyseal System</term><term>Pituitary-Adrenal System</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Pain Measurement</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Pain Threshold</term><term>Perception</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Endocrine System Diseases</term><term>Hyperalgesia</term><term>Hypothalamo-Hypophyseal System</term><term>Pain</term><term>Pituitary-Adrenal System</term></keywords><keywords scheme="MESH" type="chemical" qualifier="secretion" xml:lang="en"><term>Hydrocortisone</term><term>Hypothalamo-Hypophyseal System</term><term>Pituitary-Adrenal System</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Chronic Disease</term><term>Cross-Over Studies</term><term>Humans</term><term>Male</term><term>Young Adult</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Clinical data have accumulated showing that relative hypocortisolism, which may be regarded as a neuroendocrinological correlate of chronic stress, may be a characteristic of some functional pain syndromes. However, it has not been clarified yet whether deregulations of the hypothalamus-pituitary-adrenal (HPA) axis may directly alter pain perception and thus be causally involved in the pathophysiology of these disorders. To test this hypothesis, we performed a randomized placebo-controlled crossover trial in N=20 healthy drug-free volunteers (median age 24yrs) and analyzed the effects of metyrapone-induced hypocortisolism on quantitatively assessed basal mechanical pain sensitivity (1.5-13m/s impact stimuli), perceptual wind-up (9m/s impact stimuli at 1Hz) and temporal summation of pain elicited by inter-digital web pinching (IWP; 10N pressure stimuli for 2min). Experimentally induced hypocortisolism significantly decreased pain detection thresholds and augmented temporal summation of IWP-induced pain (p<.05). The latter effect was dependent on the relative reduction in cortisol levels, and seemed to rely on a potentiated sensitization and not merely on the observed changes in basal pain sensitivity. Perceptual wind-up by contrast was reduced when cortisol synthesis was blocked (p<.05). This result is reminiscent of findings from animal studies showing a reversal of NMDA receptor activation by glucocorticoid receptor antagonists in neuropathic pain models. Our results speak in favor of a potential causal role of HPA axis alterations in pain chronicity.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20381248</PMID><DateCreated><Year>2010</Year><Month>05</Month><Day>18</Day></DateCreated><DateCompleted><Year>2010</Year><Month>11</Month><Day>29</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-6623</ISSN><JournalIssue CitedMedium="Internet"><Volume>149</Volume><Issue>3</Issue><PubDate><Year>2010</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Pain</Title><ISOAbbreviation>Pain</ISOAbbreviation></Journal><ArticleTitle>Increased basal mechanical pain sensitivity but decreased perceptual wind-up in a human model of relative hypocortisolism.</ArticleTitle><Pagination><MedlinePgn>539-46</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.pain.2010.03.026</ELocationID><Abstract><AbstractText>Clinical data have accumulated showing that relative hypocortisolism, which may be regarded as a neuroendocrinological correlate of chronic stress, may be a characteristic of some functional pain syndromes. However, it has not been clarified yet whether deregulations of the hypothalamus-pituitary-adrenal (HPA) axis may directly alter pain perception and thus be causally involved in the pathophysiology of these disorders. To test this hypothesis, we performed a randomized placebo-controlled crossover trial in N=20 healthy drug-free volunteers (median age 24yrs) and analyzed the effects of metyrapone-induced hypocortisolism on quantitatively assessed basal mechanical pain sensitivity (1.5-13m/s impact stimuli), perceptual wind-up (9m/s impact stimuli at 1Hz) and temporal summation of pain elicited by inter-digital web pinching (IWP; 10N pressure stimuli for 2min). Experimentally induced hypocortisolism significantly decreased pain detection thresholds and augmented temporal summation of IWP-induced pain (p<.05). The latter effect was dependent on the relative reduction in cortisol levels, and seemed to rely on a potentiated sensitization and not merely on the observed changes in basal pain sensitivity. Perceptual wind-up by contrast was reduced when cortisol synthesis was blocked (p<.05). This result is reminiscent of findings from animal studies showing a reversal of NMDA receptor activation by glucocorticoid receptor antagonists in neuropathic pain models. Our results speak in favor of a potential causal role of HPA axis alterations in pain chronicity.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kuehl</LastName><ForeName>Linn K</ForeName><Initials>LK</Initials><AffiliationInfo><Affiliation>Institute of Psychobiology, Department of Clinical Physiology, University of Trier, Johanniterufer 15, Trier, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Michaux</LastName><ForeName>Gilles P</ForeName><Initials>GP</Initials></Author><Author ValidYN="Y"><LastName>Richter</LastName><ForeName>Steffen</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Schächinger</LastName><ForeName>Hartmut</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Anton</LastName><ForeName>Fernand</ForeName><Initials>F</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>04</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Pain</MedlineTA><NlmUniqueID>7508686</NlmUniqueID><ISSNLinking>0304-3959</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>WI4X0X7BPJ</RegistryNumber><NameOfSubstance UI="D006854">Hydrocortisone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002908" MajorTopicYN="N">Chronic Disease</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018592" MajorTopicYN="N">Cross-Over 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MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017288" MajorTopicYN="N">Pain Threshold</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010465" MajorTopicYN="N">Perception</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010913" MajorTopicYN="N">Pituitary-Adrenal System</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName><QualifierName UI="Q000557" MajorTopicYN="N">secretion</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055815" MajorTopicYN="N">Young Adult</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate 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