ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000D12

Evidence for impaired presynaptic dopamine function in parkinsonian patients with motor fluctuations

Identifieur interne : 000D12 ( PascalFrancis/Corpus ); précédent : 000D11; suivant : 000D13

Evidence for impaired presynaptic dopamine function in parkinsonian patients with motor fluctuations

Auteurs : R. De La Fuente-Fernandez ; P. K. Pal ; F. J. G. Vingerhoets ; A. Kishore ; M. Schulzer ; E. K. Mak ; T. J. Ruth ; B. J. Snow ; D. B. Calne ; A. J. Stoessl

Source :

Journal of neural transmission [ 0300-9564 ] ; 2000.

RBID : Pascal:00-0162255

Descripteurs français

Pascal (Inist)
- Dopamine, Présynaptique, Tomoscintigraphie, Voie nigrostriatale, Fluctuation, Motricité, Parkinson maladie, Idiopathique, Homme.

English descriptors

KwdEn :
- Dopamine, Emission tomography, Fluctuations, Human, Idiopathic, Motricity, Nigrostriatal pathway, Parkinson disease, Presynaptic.

Abstract

We used [¹⁸F]6-fluorodopa (FD) positron emission tomography (PET) to examine the severity of nigrostriatal dopaminergic dysfunction in 67 patients with Idiopathic Parkinsonism (IP), 52 with fluctuations and 15 with a stable response to levodopa. FD uptake (Ki) was reduced by 12% in the caudate (p = 0.08) and by 28% in the putamen (p = 0.0004) of patients with fluctuations compared to those with a stable response. However, there was considerable overlap of FD Ki values between the two groups. The fluctuators had a longer symptom duration (11.6 ± 5.7 years) than the patients with a stable response to levodopa (4.3 ± 2.4 years; p < 0.0001) and the age of onset of symptoms was earlier in the fluctuators (43.9 ± 8.9 versus 54.1 ± 10.4; p = 0.0004). Similar reductions in FD Ki in the fluctuators persisted following adjustment for these variables (7.5% in the caudate and 26% in the putamen; p = n.s. and 0.007, respectively). When smaller groups (n = 15 each) were matched for duration of symptoms, the reduction in caudate Ki in the fluctuators was only 1.9% (p = n.s.), but there was still a 24% reduction in putamen Ki (p = 0.05). These findings suggest that fluctuators and non-fluctuators may differ in the severity of their nigrostriatal damage and provide modest support for the hypothesis that fluctuations may in part reflect altered "buffering' capacity of dopaminergic nerve terminals. However, the considerable overlap between groups suggests that other factors such as altered postsynaptic mechanisms and/or increased turnover of dopamine may make a substantial contribution to the development of motor fluctuations.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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C01	`01`		`ENG`	@0 We used [¹⁸F]6-fluorodopa (FD) positron emission tomography (PET) to examine the severity of nigrostriatal dopaminergic dysfunction in 67 patients with Idiopathic Parkinsonism (IP), 52 with fluctuations and 15 with a stable response to levodopa. FD uptake (Ki) was reduced by 12% in the caudate (p = 0.08) and by 28% in the putamen (p = 0.0004) of patients with fluctuations compared to those with a stable response. However, there was considerable overlap of FD Ki values between the two groups. The fluctuators had a longer symptom duration (11.6 ± 5.7 years) than the patients with a stable response to levodopa (4.3 ± 2.4 years; p < 0.0001) and the age of onset of symptoms was earlier in the fluctuators (43.9 ± 8.9 versus 54.1 ± 10.4; p = 0.0004). Similar reductions in FD Ki in the fluctuators persisted following adjustment for these variables (7.5% in the caudate and 26% in the putamen; p = n.s. and 0.007, respectively). When smaller groups (n = 15 each) were matched for duration of symptoms, the reduction in caudate Ki in the fluctuators was only 1.9% (p = n.s.), but there was still a 24% reduction in putamen Ki (p = 0.05). These findings suggest that fluctuators and non-fluctuators may differ in the severity of their nigrostriatal damage and provide modest support for the hypothesis that fluctuations may in part reflect altered "buffering' capacity of dopaminergic nerve terminals. However, the considerable overlap between groups suggests that other factors such as altered postsynaptic mechanisms and/or increased turnover of dopamine may make a substantial contribution to the development of motor fluctuations.
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Format Inist (serveur)

NO :	PASCAL 00-0162255 INIST
ET :	Evidence for impaired presynaptic dopamine function in parkinsonian patients with motor fluctuations
AU :	DE LA FUENTE-FERNANDEZ (R.); PAL (P. K.); VINGERHOETS (F. J. G.); KISHORE (A.); SCHULZER (M.); MAK (E. K.); RUTH (T. J.); SNOW (B. J.); CALNE (D. B.); STOESSL (A. J.); KUHN (W.); MÜLLER (T.); KRAUS (P. H.); GERLACH (M.)
AF :	Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre/Vancouver, BC/Canada (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 8 aut., 9 aut., 10 aut.); Department of Neurology, Ruhr University Bochum, St. Josef-Hospital/Bochum/Allemagne (1 aut., 2 aut.); Neurologische Universitätsklinik, St. Josef-Hospital/Bochum/Allemagne (3 aut.); Clinical Neurochemistry, Department of Psychiatry, University of Würzburg/Allemagne (4 aut.)
DT :	Publication en série; Niveau analytique
SO :	Journal of neural transmission; ISSN 0300-9564; Coden JNTMAH; Autriche; Da. 2000; Vol. 107; No. 1; Pp. 49-57; Bibl. 1 p.3/4
LA :	Anglais
EA :	We used [¹⁸F]6-fluorodopa (FD) positron emission tomography (PET) to examine the severity of nigrostriatal dopaminergic dysfunction in 67 patients with Idiopathic Parkinsonism (IP), 52 with fluctuations and 15 with a stable response to levodopa. FD uptake (Ki) was reduced by 12% in the caudate (p = 0.08) and by 28% in the putamen (p = 0.0004) of patients with fluctuations compared to those with a stable response. However, there was considerable overlap of FD Ki values between the two groups. The fluctuators had a longer symptom duration (11.6 ± 5.7 years) than the patients with a stable response to levodopa (4.3 ± 2.4 years; p < 0.0001) and the age of onset of symptoms was earlier in the fluctuators (43.9 ± 8.9 versus 54.1 ± 10.4; p = 0.0004). Similar reductions in FD Ki in the fluctuators persisted following adjustment for these variables (7.5% in the caudate and 26% in the putamen; p = n.s. and 0.007, respectively). When smaller groups (n = 15 each) were matched for duration of symptoms, the reduction in caudate Ki in the fluctuators was only 1.9% (p = n.s.), but there was still a 24% reduction in putamen Ki (p = 0.05). These findings suggest that fluctuators and non-fluctuators may differ in the severity of their nigrostriatal damage and provide modest support for the hypothesis that fluctuations may in part reflect altered "buffering' capacity of dopaminergic nerve terminals. However, the considerable overlap between groups suggests that other factors such as altered postsynaptic mechanisms and/or increased turnover of dopamine may make a substantial contribution to the development of motor fluctuations.
CC :	002B17G
FD :	Dopamine; Présynaptique; Tomoscintigraphie; Voie nigrostriatale; Fluctuation; Motricité; Parkinson maladie; Idiopathique; Homme
FG :	Neurotransmetteur; Catécholamine; Encéphale; Système nerveux central; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative
ED :	Dopamine; Presynaptic; Emission tomography; Nigrostriatal pathway; Fluctuations; Motricity; Parkinson disease; Idiopathic; Human
EG :	Neurotransmitter; Catecholamine; Brain (vertebrata); Central nervous system; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease
SD :	Dopamina; Presináptico; Tomocentelleografía; Vía nigroestriatal; Fluctuación; Motricidad; Parkinson enfermedad; Idiopático; Hombre
LO :	INIST-7168.354000081833870040
ID :	00-0162255

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Evidence for impaired presynaptic dopamine function in parkinsonian patients with motor fluctuations</title>
<author><name sortKey="De La Fuente Fernandez, R" sort="De La Fuente Fernandez, R" uniqKey="De La Fuente Fernandez R" first="R." last="De La Fuente-Fernandez">R. De La Fuente-Fernandez</name>
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<affiliation><inist:fA14 i1="01"><s1>Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre</s1>
<s2>Vancouver, BC</s2>
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<affiliation><inist:fA14 i1="01"><s1>Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre</s1>
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<series><title level="j" type="main">Journal of neural transmission</title>
<title level="j" type="abbreviated">J. neural transm.</title>
<idno type="ISSN">0300-9564</idno>
<imprint><date when="2000">2000</date>
</imprint>
</series>
</biblStruct>
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<seriesStmt><title level="j" type="main">Journal of neural transmission</title>
<title level="j" type="abbreviated">J. neural transm.</title>
<idno type="ISSN">0300-9564</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Dopamine</term>
<term>Emission tomography</term>
<term>Fluctuations</term>
<term>Human</term>
<term>Idiopathic</term>
<term>Motricity</term>
<term>Nigrostriatal pathway</term>
<term>Parkinson disease</term>
<term>Presynaptic</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Dopamine</term>
<term>Présynaptique</term>
<term>Tomoscintigraphie</term>
<term>Voie nigrostriatale</term>
<term>Fluctuation</term>
<term>Motricité</term>
<term>Parkinson maladie</term>
<term>Idiopathique</term>
<term>Homme</term>
</keywords>
</textClass>
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</teiHeader>
<front><div type="abstract" xml:lang="en">We used [<sup>18</sup>
F]6-fluorodopa (FD) positron emission tomography (PET) to examine the severity of nigrostriatal dopaminergic dysfunction in 67 patients with Idiopathic Parkinsonism (IP), 52 with fluctuations and 15 with a stable response to levodopa. FD uptake (Ki) was reduced by 12% in the caudate (p = 0.08) and by 28% in the putamen (p = 0.0004) of patients with fluctuations compared to those with a stable response. However, there was considerable overlap of FD Ki values between the two groups. The fluctuators had a longer symptom duration (11.6 ± 5.7 years) than the patients with a stable response to levodopa (4.3 ± 2.4 years; p < 0.0001) and the age of onset of symptoms was earlier in the fluctuators (43.9 ± 8.9 versus 54.1 ± 10.4; p = 0.0004). Similar reductions in FD Ki in the fluctuators persisted following adjustment for these variables (7.5% in the caudate and 26% in the putamen; p = n.s. and 0.007, respectively). When smaller groups (n = 15 each) were matched for duration of symptoms, the reduction in caudate Ki in the fluctuators was only 1.9% (p = n.s.), but there was still a 24% reduction in putamen Ki (p = 0.05). These findings suggest that fluctuators and non-fluctuators may differ in the severity of their nigrostriatal damage and provide modest support for the hypothesis that fluctuations may in part reflect altered "buffering' capacity of dopaminergic nerve terminals. However, the considerable overlap between groups suggests that other factors such as altered postsynaptic mechanisms and/or increased turnover of dopamine may make a substantial contribution to the development of motor fluctuations.</div>
</front>
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<fA08 i1="01" i2="1" l="ENG"><s1>Evidence for impaired presynaptic dopamine function in parkinsonian patients with motor fluctuations</s1>
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<fA09 i1="01" i2="1" l="ENG"><s1>Parkinson's Disease: Progress in Neurodegenerative and Clinical Research</s1>
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<fA14 i1="01"><s1>Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre</s1>
<s2>Vancouver, BC</s2>
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<fC01 i1="01" l="ENG"><s0>We used [<sup>18</sup>
F]6-fluorodopa (FD) positron emission tomography (PET) to examine the severity of nigrostriatal dopaminergic dysfunction in 67 patients with Idiopathic Parkinsonism (IP), 52 with fluctuations and 15 with a stable response to levodopa. FD uptake (Ki) was reduced by 12% in the caudate (p = 0.08) and by 28% in the putamen (p = 0.0004) of patients with fluctuations compared to those with a stable response. However, there was considerable overlap of FD Ki values between the two groups. The fluctuators had a longer symptom duration (11.6 ± 5.7 years) than the patients with a stable response to levodopa (4.3 ± 2.4 years; p < 0.0001) and the age of onset of symptoms was earlier in the fluctuators (43.9 ± 8.9 versus 54.1 ± 10.4; p = 0.0004). Similar reductions in FD Ki in the fluctuators persisted following adjustment for these variables (7.5% in the caudate and 26% in the putamen; p = n.s. and 0.007, respectively). When smaller groups (n = 15 each) were matched for duration of symptoms, the reduction in caudate Ki in the fluctuators was only 1.9% (p = n.s.), but there was still a 24% reduction in putamen Ki (p = 0.05). These findings suggest that fluctuators and non-fluctuators may differ in the severity of their nigrostriatal damage and provide modest support for the hypothesis that fluctuations may in part reflect altered "buffering' capacity of dopaminergic nerve terminals. However, the considerable overlap between groups suggests that other factors such as altered postsynaptic mechanisms and/or increased turnover of dopamine may make a substantial contribution to the development of motor fluctuations.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17G</s0>
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<s5>01</s5>
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<s2>NK</s2>
<s2>FR</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Présynaptique</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Presynaptic</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Presináptico</s0>
<s5>02</s5>
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<fC03 i1="03" i2="X" l="FRE"><s0>Tomoscintigraphie</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Emission tomography</s0>
<s5>04</s5>
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<fC03 i1="03" i2="X" l="SPA"><s0>Tomocentelleografía</s0>
<s5>04</s5>
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<fC03 i1="04" i2="X" l="FRE"><s0>Voie nigrostriatale</s0>
<s5>05</s5>
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<s5>05</s5>
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<s5>05</s5>
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<s5>06</s5>
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<s5>07</s5>
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<fC03 i1="07" i2="X" l="FRE"><s0>Parkinson maladie</s0>
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<fC03 i1="09" i2="X" l="FRE"><s0>Homme</s0>
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<s5>41</s5>
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<s5>41</s5>
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<s5>42</s5>
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<fC07 i1="09" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>42</s5>
</fC07>
<fN21><s1>115</s1>
</fN21>
</pA>
</standard>
<server><NO>PASCAL 00-0162255 INIST</NO>
<ET>Evidence for impaired presynaptic dopamine function in parkinsonian patients with motor fluctuations</ET>
<AU>DE LA FUENTE-FERNANDEZ (R.); PAL (P. K.); VINGERHOETS (F. J. G.); KISHORE (A.); SCHULZER (M.); MAK (E. K.); RUTH (T. J.); SNOW (B. J.); CALNE (D. B.); STOESSL (A. J.); KUHN (W.); MÜLLER (T.); KRAUS (P. H.); GERLACH (M.)</AU>
<AF>Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre/Vancouver, BC/Canada (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 8 aut., 9 aut., 10 aut.); Department of Neurology, Ruhr University Bochum, St. Josef-Hospital/Bochum/Allemagne (1 aut., 2 aut.); Neurologische Universitätsklinik, St. Josef-Hospital/Bochum/Allemagne (3 aut.); Clinical Neurochemistry, Department of Psychiatry, University of Würzburg/Allemagne (4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of neural transmission; ISSN 0300-9564; Coden JNTMAH; Autriche; Da. 2000; Vol. 107; No. 1; Pp. 49-57; Bibl. 1 p.3/4</SO>
<LA>Anglais</LA>
<EA>We used [<sup>18</sup>
F]6-fluorodopa (FD) positron emission tomography (PET) to examine the severity of nigrostriatal dopaminergic dysfunction in 67 patients with Idiopathic Parkinsonism (IP), 52 with fluctuations and 15 with a stable response to levodopa. FD uptake (Ki) was reduced by 12% in the caudate (p = 0.08) and by 28% in the putamen (p = 0.0004) of patients with fluctuations compared to those with a stable response. However, there was considerable overlap of FD Ki values between the two groups. The fluctuators had a longer symptom duration (11.6 ± 5.7 years) than the patients with a stable response to levodopa (4.3 ± 2.4 years; p < 0.0001) and the age of onset of symptoms was earlier in the fluctuators (43.9 ± 8.9 versus 54.1 ± 10.4; p = 0.0004). Similar reductions in FD Ki in the fluctuators persisted following adjustment for these variables (7.5% in the caudate and 26% in the putamen; p = n.s. and 0.007, respectively). When smaller groups (n = 15 each) were matched for duration of symptoms, the reduction in caudate Ki in the fluctuators was only 1.9% (p = n.s.), but there was still a 24% reduction in putamen Ki (p = 0.05). These findings suggest that fluctuators and non-fluctuators may differ in the severity of their nigrostriatal damage and provide modest support for the hypothesis that fluctuations may in part reflect altered "buffering' capacity of dopaminergic nerve terminals. However, the considerable overlap between groups suggests that other factors such as altered postsynaptic mechanisms and/or increased turnover of dopamine may make a substantial contribution to the development of motor fluctuations.</EA>
<CC>002B17G</CC>
<FD>Dopamine; Présynaptique; Tomoscintigraphie; Voie nigrostriatale; Fluctuation; Motricité; Parkinson maladie; Idiopathique; Homme</FD>
<FG>Neurotransmetteur; Catécholamine; Encéphale; Système nerveux central; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative</FG>
<ED>Dopamine; Presynaptic; Emission tomography; Nigrostriatal pathway; Fluctuations; Motricity; Parkinson disease; Idiopathic; Human</ED>
<EG>Neurotransmitter; Catecholamine; Brain (vertebrata); Central nervous system; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease</EG>
<SD>Dopamina; Presináptico; Tomocentelleografía; Vía nigroestriatal; Fluctuación; Motricidad; Parkinson enfermedad; Idiopático; Hombre</SD>
<LO>INIST-7168.354000081833870040</LO>
<ID>00-0162255</ID>
</server>
</inist>
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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

Evidence for impaired presynaptic dopamine function in parkinsonian patients with motor fluctuations

Evidence for impaired presynaptic dopamine function in parkinsonian patients with motor fluctuations

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