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dc.contributor.author
Vuilleumier, Pascal Henri
dc.contributor.author
Fritsche, Raphael
dc.contributor.author
Schliessbach, Jürg
dc.contributor.author
Schmitt, Bernhard
dc.contributor.author
Arendt-Nielsen, Lars
dc.contributor.author
Zeilhofer, Hanns U.
dc.contributor.author
Curatolo, Michele
dc.date.accessioned
2023-09-19T08:24:41Z
dc.date.available
2018-01-26T08:59:13Z
dc.date.available
2018-02-05T15:28:58Z
dc.date.available
2018-01-25T02:53:41Z
dc.date.available
2023-09-19T08:24:41Z
dc.date.issued
2018-01
dc.identifier.issn
0006-8950
dc.identifier.issn
1460-2156
dc.identifier.other
10.1093/brain/awx289
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/238896
dc.identifier.doi
10.3929/ethz-b-000238896
dc.description.abstract
Inhibitory interneurons in the spinal cord use glycine and GABA for fast inhibitory neurotransmission. While there is abundant research on these inhibitory pain pathways in animal models, their relevance in humans remains unclear, largely due to the limited possibility to manipulate selectively these pathways in humans. Hyperekplexia is a rare human disease that is caused by loss-of-function mutations in genes encoding for glycine receptors and glycine transporters. In the present study, we tested whether hyperekplexia patients display altered pain perception or central pain modulation compared with healthy subjects. Seven patients with genetically and clinically confirmed hyperekplexia were compared to 14 healthy age- and sex-matched controls. The following quantitative sensory tests were performed: pressure pain detection threshold (primary outcome), ice water tolerance, single and repeated electrical pain detection thresholds, nociceptive withdrawal reflex threshold, and conditioned pain modulation. Statistical analysis was performed using linear mixed models. Hyperekplexia patients displayed lower pain thresholds than healthy controls for all of the quantitative sensory tests [mean (standard deviation)]: pressure pain detection threshold [273 (170) versus 475 (115) kPa, P = 0.003], ice water tolerance [49.2 (36.5) versus 85.7 (35.0) s, P = 0.015], electrical single pain detection threshold [5.42 (2.64) versus 7.47 (2.62) mA, P = 0.012], electrical repeated pain detection threshold [3.76 (1.41) versus 5.8 (1.73) mA, P = 0.003], and nociceptive withdrawal reflex [7.42 (3.63) versus 14.1 (6.9) mA, P = 0.015]. Conditioned pain modulation was significantly reduced in hyperekplexia [increase to baseline: 53.2 (63.7) versus 105 (57) kPa, P = 0.030]. Our data demonstrate increased pain sensitivity and impaired central pain modulation in hyperekplexia patients, supporting the importance of glycinergic neurotransmission for central pain modulation in humans.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Oxford University Press
en_US
dc.rights.uri
http://rightsstatements.org/page/InC-NC/1.0/
dc.subject
hyperekplexia
en_US
dc.subject
GABA
en_US
dc.subject
glycine
en_US
dc.subject
startle disease
en_US
dc.subject
pain modulation
en_US
dc.title
Mutations affecting glycinergic neurotransmission in hyperekplexia increase pain sensitivity
en_US
dc.type
Journal Article
dc.rights.license
In Copyright - Non-Commercial Use Permitted
dc.date.published
2017-11-15
ethz.journal.title
Brain: A Journal of Neurology
ethz.journal.volume
141
en_US
ethz.journal.issue
1
en_US
ethz.journal.abbreviated
Brain
ethz.pages.start
63
en_US
ethz.pages.end
71
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.notes
It was possible to publish this article open access thanks to a Swiss National Licence with the publisher.
en_US
ethz.identifier.wos
ethz.identifier.scopus
ethz.publication.place
Oxford
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02020 - Dep. Chemie und Angewandte Biowiss. / Dep. of Chemistry and Applied Biosc.::02534 - Institut für Pharmazeutische Wiss. / Institute of Pharmaceutical Sciences::03742 - Zeilhofer, Hanns U. / Zeilhofer, Hanns U.
en_US
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02020 - Dep. Chemie und Angewandte Biowiss. / Dep. of Chemistry and Applied Biosc.::02534 - Institut für Pharmazeutische Wiss. / Institute of Pharmaceutical Sciences::03742 - Zeilhofer, Hanns U. / Zeilhofer, Hanns U.
en_US
ethz.date.deposited
2018-01-25T02:54:00Z
ethz.source
FORM
ethz.source
WOS
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2018-02-06T09:45:13Z
ethz.rosetta.lastUpdated
2024-02-03T03:51:57Z
ethz.rosetta.versionExported
true
dc.identifier.olduri
http://hdl.handle.net/20.500.11850/234014
dc.identifier.olduri
http://hdl.handle.net/20.500.11850/235032
ethz.COinS
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