Acute and long-term administration of anticholinergics in Parkinson's disease: specific effects on the subcortico-frontal syndrome.
Identifieur interne : 003C04 ( Main/Merge ); précédent : 003C03; suivant : 003C05Acute and long-term administration of anticholinergics in Parkinson's disease: specific effects on the subcortico-frontal syndrome.
Auteurs : M A Bédard [Canada] ; B. Pillon ; B. Dubois ; N. Duchesne ; H. Masson ; Yves Agid [France]Source :
- Brain and cognition [ 0278-2626 ] ; 1999.
English descriptors
- KwdEn :
- Acute Disease, Cholinergic Antagonists (therapeutic use), Cognition Disorders (chemically induced), Cognition Disorders (diagnosis), Corpus Striatum (pathology), Cross-Over Studies, Dose-Response Relationship, Drug, Double-Blind Method, Humans, Levodopa (therapeutic use), Middle Aged, Nerve Degeneration, Neuropsychological Tests, Parkinson Disease (drug therapy), Parkinson Disease (pathology), Scopolamine Hydrobromide (adverse effects), Severity of Illness Index, Substantia Nigra (pathology), Syndrome, Time Factors, Trihexyphenidyl (adverse effects).
- MESH :
- chemical , adverse effects : Scopolamine Hydrobromide, Trihexyphenidyl.
- chemical , therapeutic use : Cholinergic Antagonists, Levodopa.
- chemically induced : Cognition Disorders.
- diagnosis : Cognition Disorders.
- drug therapy : Parkinson Disease.
- pathology : Corpus Striatum, Parkinson Disease, Substantia Nigra.
- Acute Disease, Cross-Over Studies, Dose-Response Relationship, Drug, Double-Blind Method, Humans, Middle Aged, Nerve Degeneration, Neuropsychological Tests, Severity of Illness Index, Syndrome, Time Factors.
Abstract
Parkinson's Disease (PD) is often associated with a subcortico-frontal syndrome (SCFS) that is mainly characterized by executive dysfunctions. The complete biochemistry of these dysfunctions remain misunderstood. Most studies have focused on the well-known nigro-striatal dopaminergic degenerations of PD, but a more satisfying understanding of the SCFS has come from the study of the cholinergic systems. We present here two new experiments carried out with long-term and acute anticholinergic treatments in PD. In the first experiment, the effects of a 2-week treatment with trihexyphenidyl were compared to those observed under placebo on a neuropsychological battery. Results showed that anticholinergic-induced deficits in PD were exclusively concerned with executive functions. In the second experiment, the effects of an acute subclinical dose of scopolamine were compared between normal controls and PD patients who were devoid of cognitive deficit on a subset of executive tasks. Results indicates that PD patients but not normal controls developed a transient SCFS for the duration of the drug action. In contrast to other populations with cholinergic depletions-such as Alzheimer's disease-cholinergic blockade in PD exacerbates specifically the SCFS. Such a discrepancy between these two neuropsychological profiles are discussed in terms of the specificity of the underlying cholinergic lesions.
DOI: 10.1006/brcg.1999.1083
PubMed: 10413563
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pubmed:10413563Le document en format XML
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<front><div type="abstract" xml:lang="en">Parkinson's Disease (PD) is often associated with a subcortico-frontal syndrome (SCFS) that is mainly characterized by executive dysfunctions. The complete biochemistry of these dysfunctions remain misunderstood. Most studies have focused on the well-known nigro-striatal dopaminergic degenerations of PD, but a more satisfying understanding of the SCFS has come from the study of the cholinergic systems. We present here two new experiments carried out with long-term and acute anticholinergic treatments in PD. In the first experiment, the effects of a 2-week treatment with trihexyphenidyl were compared to those observed under placebo on a neuropsychological battery. Results showed that anticholinergic-induced deficits in PD were exclusively concerned with executive functions. In the second experiment, the effects of an acute subclinical dose of scopolamine were compared between normal controls and PD patients who were devoid of cognitive deficit on a subset of executive tasks. Results indicates that PD patients but not normal controls developed a transient SCFS for the duration of the drug action. In contrast to other populations with cholinergic depletions-such as Alzheimer's disease-cholinergic blockade in PD exacerbates specifically the SCFS. Such a discrepancy between these two neuropsychological profiles are discussed in terms of the specificity of the underlying cholinergic lesions.</div>
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