Movement Disorders (revue)

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The autonomic nervous system in Gilles de la Tourette's syndrome

Identifieur interne : 006598 ( Main/Exploration ); précédent : 006597; suivant : 006599

The autonomic nervous system in Gilles de la Tourette's syndrome

Auteurs : Goetz [États-Unis] ; Kathleen M. Shannon [États-Unis] ; V. Susan Carroll [États-Unis] ; Caroline M. Tanner [États-Unis] ; Randall Weingarten [États-Unis]

Source :

RBID : ISTEX:03AE769DC83E25EB1D917B142175E3617C3D3A14

English descriptors

Abstract

Twenty‐three patients with Gilles de la Tourette's syndromes (GTS) underwent nonivasive 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 <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 neuroleptoc 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.

Url:
DOI: 10.1002/mds.870020203


Affiliations:


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Le document en format XML

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<term>Autonomic Nervous System (physiopathology)</term>
<term>Autonomic nervous system</term>
<term>Cardiovascular system</term>
<term>Clonidine</term>
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<term>Female</term>
<term>Gilles de la Tourette's syndrome</term>
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<div type="abstract" xml:lang="en">Twenty‐three patients with Gilles de la Tourette's syndromes (GTS) underwent nonivasive 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 <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 neuroleptoc 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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