MovDisordV3, Main, Exploration, bibRecord, 003C30

Opioid binding in DYT1 primary torsion dystonia: An 11C‐diprenorphine PET study

Identifieur interne : 003C30 ( Main/Exploration ); précédent : 003C29; suivant : 003C31

Opioid binding in DYT1 primary torsion dystonia: An 11C‐diprenorphine PET study

Auteurs : Alan L. Whone [Royaume-Uni] ; Sarah Von Spiczak [Royaume-Uni] ; Mark Edwards [Royaume-Uni] ; Enza-Maria Valente [Royaume-Uni] ; Alexander Hammers [Royaume-Uni] ; Kailash P. Bhatia [Royaume-Uni] ; David J. Brooks [Royaume-Uni]

Source :

Movement Disorders [ 0885-3185 ] ; 2004-12.

RBID : ISTEX:1F7FDD7A5B5C9D934F50EE63C025334FDD231811

Descripteurs français

Pascal (Inist)
- Contrôle moteur, Diprénorphine, Dystonie, Exploration radioisotopique, Positon, Système nerveux pathologie, Tomographie émission positon, Tomoscintigraphie, Torsion.

English descriptors

KwdEn :
- 11C‐diprenorphine, Adult, Aged, Basal Ganglia (metabolism), Binding Sites, Corpus Striatum (metabolism), DYT1, Diprenorphine, Diprenorphine (administration & dosage), Diprenorphine (pharmacokinetics), Dystonia, Dystonia Musculorum Deformans (genetics), Dystonia Musculorum Deformans (metabolism), Emission tomography, Enkephalins (metabolism), Female, Gene Deletion, Humans, Male, Middle Aged, Molecular Chaperones (genetics), Motor control, Nervous system diseases, Positron, Positron emission tomography, Positron-Emission Tomography, Radionuclide study, Severity of Illness Index, Torsion, dystonia, opioid.
MESH :
- chemical , administration & dosage : Diprenorphine.
- genetics : Dystonia Musculorum Deformans, Molecular Chaperones.
- metabolism : Basal Ganglia, Corpus Striatum, Dystonia Musculorum Deformans, Enkephalins.
- chemical , pharmacokinetics : Diprenorphine.
- Adult, Aged, Binding Sites, Female, Gene Deletion, Humans, Male, Middle Aged, Positron-Emission Tomography, Severity of Illness Index.

Abstract

The opioid transmitters enkephalin and dynorphin are known to regulate pallidal output and consequently cortical excitability. Indeed, abnormal basal ganglia opioid transmission has been reported in several involuntary movement disorders, including levodopa‐induced dyskinesias in Parkinson's disease (PD), tardive dyskinesias/dystonia, Huntington's disease, and Tourette's syndrome. Moreover, a previous 11C‐diprenorphine PET study investigating levodopa‐induced dyskinesias found reduced opioid receptor availability in PD with but not without dyskinesias. We wished to investigate if a similar alteration in basal ganglia opioid binding was present in DYT1 primary torsion dystonia (PTD). Regional cerebral 11C‐diprenorphine binding was investigated in 7 manifesting carriers of the DYT1 gene and 15 age‐matched normal controls using a region‐of‐interest (ROI) approach and statistical parametric mapping (SPM). No difference in regional mean 11C‐diprenorphine binding was found between DYT1‐PTD and controls, and no correlation between the severity of dystonia and opioid binding was seen. We conclude that aberrant opioid transmission is unlikely to be present in DYT1‐PTD and altered opioid transmission is not a common mechanism underlying all disorders of involuntary movement. © 2004 Movement Disorder Society

Url:

https://api.istex.fr/document/1F7FDD7A5B5C9D934F50EE63C025334FDD231811/fulltext/pdf

DOI: 10.1002/mds.20238

Affiliations:

Le document en format XML

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<front><div type="abstract" xml:lang="en">The opioid transmitters enkephalin and dynorphin are known to regulate pallidal output and consequently cortical excitability. Indeed, abnormal basal ganglia opioid transmission has been reported in several involuntary movement disorders, including levodopa‐induced dyskinesias in Parkinson's disease (PD), tardive dyskinesias/dystonia, Huntington's disease, and Tourette's syndrome. Moreover, a previous 11C‐diprenorphine PET study investigating levodopa‐induced dyskinesias found reduced opioid receptor availability in PD with but not without dyskinesias. We wished to investigate if a similar alteration in basal ganglia opioid binding was present in DYT1 primary torsion dystonia (PTD). Regional cerebral 11C‐diprenorphine binding was investigated in 7 manifesting carriers of the DYT1 gene and 15 age‐matched normal controls using a region‐of‐interest (ROI) approach and statistical parametric mapping (SPM). No difference in regional mean 11C‐diprenorphine binding was found between DYT1‐PTD and controls, and no correlation between the severity of dystonia and opioid binding was seen. We conclude that aberrant opioid transmission is unlikely to be present in DYT1‐PTD and altered opioid transmission is not a common mechanism underlying all disorders of involuntary movement. © 2004 Movement Disorder Society</div>
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Movement Disorders (revue)

Opioid binding in DYT1 primary torsion dystonia: An 11C‐diprenorphine PET study

Opioid binding in DYT1 primary torsion dystonia: An 11C‐diprenorphine PET study

Source :

Descripteurs français

English descriptors

Abstract

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