The autonomic nervous system in Gilles de la Tourette's syndrome.
Identifieur interne : 004564 ( Ncbi/Curation ); précédent : 004563; suivant : 004565The autonomic nervous system in Gilles de la Tourette's syndrome.
Auteurs : C G Goetz [États-Unis] ; K M Shannon ; V S Carroll ; C M Tanner ; R. WeingartenSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1987.
English descriptors
- KwdEn :
- MESH :
- chemical , pharmacology : Antipsychotic Agents, Clonidine.
- drug effects : Autonomic Nervous System.
- drug therapy : Tourette Syndrome.
- physiopathology : Autonomic Nervous System, Tourette Syndrome.
- Adolescent, Adult, Drug Therapy, Combination, Female, Humans, Male.
Abstract
Twenty-three patients with Gilles de la Tourette's syndrome (GTS) underwent noninvasive investigation of autonomic nervous system (ANS) function, as did 23 age-matched controls. ANS function in GTS patients was no different from that of controls, and patients receiving neuroleptic drugs had the same ANS function as untreated patients. All 23 patients later received clonidine and were retested. The ANS values before administration of clonidine were compared with those while patients were taking clonidine. The only significant change (p less than 0.01) with clonidine was a reduced resting pulse rate. The combination of clonidine and neuroleptic drugs did not induce significant autonomic changes compared with neuroleptic therapy alone. These results indicate that the ANS in GTS patients is normal and that the drugs used to abate tics do not produce clinically significant changes in ANS when chronically given. The findings suggest that the pathophysiology and treatment of GTS do not directly involve the nuclei or tracts of autonomic regulation.
DOI: 10.1002/mds.870020203
PubMed: 2904121
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pubmed:2904121Le document en format XML
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<author><name sortKey="Goetz, C G" sort="Goetz, C G" uniqKey="Goetz C" first="C G" last="Goetz">C G Goetz</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Neurological Sciences, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois 60612.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Illinois</region>
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<wicri:cityArea>Department of Neurological Sciences, Rush-Presbyterian-St. Luke's Medical Center, Chicago</wicri:cityArea>
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<author><name sortKey="Shannon, K M" sort="Shannon, K M" uniqKey="Shannon K" first="K M" last="Shannon">K M Shannon</name>
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<author><name sortKey="Carroll, V S" sort="Carroll, V S" uniqKey="Carroll V" first="V S" last="Carroll">V S Carroll</name>
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<author><name sortKey="Tanner, C M" sort="Tanner, C M" uniqKey="Tanner C" first="C M" last="Tanner">C M Tanner</name>
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<author><name sortKey="Weingarten, R" sort="Weingarten, R" uniqKey="Weingarten R" first="R" last="Weingarten">R. Weingarten</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">The autonomic nervous system in Gilles de la Tourette's syndrome.</title>
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<affiliation wicri:level="2"><nlm:affiliation>Department of Neurological Sciences, Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois 60612.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
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<author><name sortKey="Tanner, C M" sort="Tanner, C M" uniqKey="Tanner C" first="C M" last="Tanner">C M Tanner</name>
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<series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
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<term>Autonomic Nervous System (physiopathology)</term>
<term>Clonidine (pharmacology)</term>
<term>Drug Therapy, Combination</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Tourette Syndrome (drug therapy)</term>
<term>Tourette Syndrome (physiopathology)</term>
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<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Autonomic Nervous System</term>
<term>Tourette Syndrome</term>
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<front><div type="abstract" xml:lang="en">Twenty-three patients with Gilles de la Tourette's syndrome (GTS) underwent noninvasive investigation of autonomic nervous system (ANS) function, as did 23 age-matched controls. ANS function in GTS patients was no different from that of controls, and patients receiving neuroleptic drugs had the same ANS function as untreated patients. All 23 patients later received clonidine and were retested. The ANS values before administration of clonidine were compared with those while patients were taking clonidine. The only significant change (p less than 0.01) with clonidine was a reduced resting pulse rate. The combination of clonidine and neuroleptic drugs did not induce significant autonomic changes compared with neuroleptic therapy alone. These results indicate that the ANS in GTS patients is normal and that the drugs used to abate tics do not produce clinically significant changes in ANS when chronically given. The findings suggest that the pathophysiology and treatment of GTS do not directly involve the nuclei or tracts of autonomic regulation.</div>
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