Serveur d'exploration sur la maladie de Parkinson

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Deep brain stimulation in the treatment of Parkinson's disease: a review and update

Identifieur interne : 000863 ( Main/Corpus ); précédent : 000862; suivant : 000864

Deep brain stimulation in the treatment of Parkinson's disease: a review and update

Auteurs : Patricia Dowsey-Limousin ; Pierre Pollak

Source :

RBID : ISTEX:DB8891786BF537B5B60452C25BC70502061DF52E

English descriptors

Abstract

Deep brain stimulation (DBS) is a neurosurgical treatment of severe forms of Parkinson's disease, already applied to three targets, the thalamus, the internal pallidum (GPi) and the subthalamic nucleus (STN). Thalamic DBS mainly improves contralateral tremor and is therefore restricted to a small group of patients with tremor dominant disease. STN and GPi DBS improve off-motor periods and dyskinesias. The magnitude of the improvement seems more constant with STN DBS than with GPi, but there is very little comparative data between these procedures. The DBS procedure has the unique advantage of reversibility and adjustability over time. Most authors agree that bilateral DBS is reasonably safe, which is not the case of ablation. In any event, surgery is restricted to patients disabled by their condition but still responding well at times to levodopa, who are generally fit with no behavioural, mood or cognitive impairment. DBS can have side effects. Side effects more specific to the DBS procedure are infection, disconnection and hardware failure. DBS, like ablative surgery can induce an intracranial lesion like a hematoma or a stroke. There are side effects more specific to the target like postural instability, dysarthria or paresthesia in the thalamus and dyskinesias or eyelid opening apraxia in the STN. The mechanism by which high frequency DBS mimics the effect of ablation is not fully understood.

Url:
DOI: 10.1016/S1566-2772(01)00029-9

Links to Exploration step

ISTEX:DB8891786BF537B5B60452C25BC70502061DF52E

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<abstract lang="en">Deep brain stimulation (DBS) is a neurosurgical treatment of severe forms of Parkinson's disease, already applied to three targets, the thalamus, the internal pallidum (GPi) and the subthalamic nucleus (STN). Thalamic DBS mainly improves contralateral tremor and is therefore restricted to a small group of patients with tremor dominant disease. STN and GPi DBS improve off-motor periods and dyskinesias. The magnitude of the improvement seems more constant with STN DBS than with GPi, but there is very little comparative data between these procedures. The DBS procedure has the unique advantage of reversibility and adjustability over time. Most authors agree that bilateral DBS is reasonably safe, which is not the case of ablation. In any event, surgery is restricted to patients disabled by their condition but still responding well at times to levodopa, who are generally fit with no behavioural, mood or cognitive impairment. DBS can have side effects. Side effects more specific to the DBS procedure are infection, disconnection and hardware failure. DBS, like ablative surgery can induce an intracranial lesion like a hematoma or a stroke. There are side effects more specific to the target like postural instability, dysarthria or paresthesia in the thalamus and dyskinesias or eyelid opening apraxia in the STN. The mechanism by which high frequency DBS mimics the effect of ablation is not fully understood.</abstract>
<subject lang="en">
<genre>Keywords</genre>
<topic>Deep brain stimulation</topic>
<topic>Thalamus</topic>
<topic>Internal pallidum</topic>
<topic>Subthalamic nucleus</topic>
<topic>Parkinson's disease</topic>
<topic>Surgical treatment</topic>
</subject>
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<title>Clinical Neuroscience Research</title>
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<titleInfo type="abbreviated">
<title>CLIRES</title>
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<genre type="Journal">journal</genre>
<originInfo>
<dateIssued encoding="w3cdtf">200112</dateIssued>
</originInfo>
<identifier type="ISSN">1566-2772</identifier>
<identifier type="PII">S1566-2772(00)X0005-9</identifier>
<part>
<date>200112</date>
<detail type="issue">
<title>Advances in Parkinson's Disease Research</title>
</detail>
<detail type="volume">
<number>1</number>
<caption>vol.</caption>
</detail>
<detail type="issue">
<number>6</number>
<caption>no.</caption>
</detail>
<extent unit="issue pages">
<start>405</start>
<end>540</end>
</extent>
<extent unit="pages">
<start>521</start>
<end>526</end>
</extent>
</part>
</relatedItem>
<identifier type="istex">DB8891786BF537B5B60452C25BC70502061DF52E</identifier>
<identifier type="DOI">10.1016/S1566-2772(01)00029-9</identifier>
<identifier type="PII">S1566-2772(01)00029-9</identifier>
<accessCondition type="use and reproduction" contentType="">© 2001Elsevier Science B.V.</accessCondition>
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<recordContentSource>ELSEVIER</recordContentSource>
<recordOrigin>Elsevier Science B.V., ©2001</recordOrigin>
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<classCode scheme="WOS">CLINICAL NEUROLOGY</classCode>
<classCode scheme="WOS">NEUROSCIENCES</classCode>
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