Reduced glutamate decarboxylase activity in the subthalamic nucleus in patients with tardive dyskinesia
Identifieur interne : 006433 ( Main/Exploration ); précédent : 006432; suivant : 006434Reduced glutamate decarboxylase activity in the subthalamic nucleus in patients with tardive dyskinesia
Auteurs : Ulf Andersson [Suède] ; Jan-Erik H Gström [Suède] ; Edward D. Levin [Suède] ; Ulf Bondesson [Suède] ; Milan Valverius [Suède] ; Gunne [Suède]Source :
- Movement Disorders [ 0885-3185 ] ; 1989.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Death, Sudden (pathology), Dyskinesia, Dyskinesia, Drug-Induced (pathology), Enzymatic activity, Female, GABA, GAD‐activity, Glutamate Decarboxylase (deficiency), Glutamate decarboxylase, Human, Humans, Involuntary movement, Male, Middle Aged, Myocardial Infarction (pathology), Nervous system diseases, Neuroleptic, Psychotropic, Subthalamic nucleus, Tardive dyskinesia, Thalamic Nuclei (pathology), Toxicity.
- MESH :
- chemical , deficiency : Glutamate Decarboxylase.
- pathology : Death, Sudden, Dyskinesia, Drug-Induced, Myocardial Infarction, Thalamic Nuclei.
- Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged.
Abstract
Glutamate decarboxylase (GAD) activity was measured in the nuclei of the basal ganglia in patients with neuroleptic‐induced tardive dyskinesia (TD) and controls matched for age and premortem state. In five TD patients, who all had a sudden death, a significant decrease in GAD activity was found in the subthalamic nucleus (STN). The lowered GAD activity in the STN may represent a biochemical substrate for neuroleptic‐induced TD.
Url:
DOI: 10.1002/mds.870040107
Affiliations:
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Le document en format XML
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<series><title level="j">Movement Disorders</title>
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<term>Aged, 80 and over</term>
<term>Death, Sudden (pathology)</term>
<term>Dyskinesia</term>
<term>Dyskinesia, Drug-Induced (pathology)</term>
<term>Enzymatic activity</term>
<term>Female</term>
<term>GABA</term>
<term>GAD‐activity</term>
<term>Glutamate Decarboxylase (deficiency)</term>
<term>Glutamate decarboxylase</term>
<term>Human</term>
<term>Humans</term>
<term>Involuntary movement</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Myocardial Infarction (pathology)</term>
<term>Nervous system diseases</term>
<term>Neuroleptic</term>
<term>Psychotropic</term>
<term>Subthalamic nucleus</term>
<term>Tardive dyskinesia</term>
<term>Thalamic Nuclei (pathology)</term>
<term>Toxicity</term>
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<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Glutamate Decarboxylase</term>
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<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Death, Sudden</term>
<term>Dyskinesia, Drug-Induced</term>
<term>Myocardial Infarction</term>
<term>Thalamic Nuclei</term>
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<keywords scheme="MESH" xml:lang="en"><term>Aged</term>
<term>Aged, 80 and over</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Activité enzymatique</term>
<term>Dyskinésie</term>
<term>GABA</term>
<term>Glutamate decarboxylase</term>
<term>Homme</term>
<term>Mouvement involontaire</term>
<term>Neuroleptique</term>
<term>Noyau sousthalamique</term>
<term>Psychotrope</term>
<term>Système nerveux pathologie</term>
<term>Toxicité</term>
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<front><div type="abstract" xml:lang="en">Glutamate decarboxylase (GAD) activity was measured in the nuclei of the basal ganglia in patients with neuroleptic‐induced tardive dyskinesia (TD) and controls matched for age and premortem state. In five TD patients, who all had a sudden death, a significant decrease in GAD activity was found in the subthalamic nucleus (STN). The lowered GAD activity in the STN may represent a biochemical substrate for neuroleptic‐induced TD.</div>
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<name sortKey="H Gstrom, Jan Rik" sort="H Gstrom, Jan Rik" uniqKey="H Gstrom J" first="Jan-Erik" last="H Gström">Jan-Erik H Gström</name>
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<name sortKey="Valverius, Milan" sort="Valverius, Milan" uniqKey="Valverius M" first="Milan" last="Valverius">Milan Valverius</name>
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