[11C]RTI-32 PET studies of the dopamine transporter in early dopa-naive Parkinson's disease : Implications for the symptomatic threshold
Identifieur interne : 000E67 ( PascalFrancis/Corpus ); précédent : 000E66; suivant : 000E68[11C]RTI-32 PET studies of the dopamine transporter in early dopa-naive Parkinson's disease : Implications for the symptomatic threshold
Auteurs : M. Guttman ; J. Burkholder ; S. J. Kish ; D. Hussey ; A. Wilson ; J. Dasilva ; S. HouleSource :
- Neurology [ 0028-3878 ] ; 1997.
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- Pascal (Inist)
English descriptors
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Abstract
Article abstract-To estimate the threshold of nigrostriatal dysfunction required for symptomatic Parkinson's disease (PD), we employed [11C ]RTI-32 and PET to study the dopamine transporter in striatal subdivisions of 11 L-dopa-naive patients with very early parkinsonism. As compared with the controls (N = 10), the PD group had on the side contralateral to the maximal clinical symptoms, significantly reduced binding in the posterior putamen (-56%) and anterior putamen (-28%), with the reduction in caudate (- 12%) not significantly different. To the extent that dopamine transporter binding accurately reflects the number of nigrostriatal dopamine nerve terminals, these findings suggest that the clinical threshold for PD in the middle-age human is approximately 50% loss of dopaminergic innervation to the posterior putamen. Our data also suggest that damage to the putamen component of the striatum is sufficient for the clinical expression of PD.
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Pour connaître la documentation sur le format Inist Standard.
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Format Inist (serveur)
NO : | PASCAL 97-0355687 INIST |
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ET : | [11C]RTI-32 PET studies of the dopamine transporter in early dopa-naive Parkinson's disease : Implications for the symptomatic threshold |
AU : | GUTTMAN (M.); BURKHOLDER (J.); KISH (S. J.); HUSSEY (D.); WILSON (A.); DASILVA (J.); HOULE (S.) |
AF : | Human Neurochemical Pathology Laboratory/Canada (1 aut., 3 aut.); Clarke Institute of Psychiatry, Division of Neurology, University of Toronto Faculty of Medicine/Toronto, Ontario/Canada (1 aut.); PET Center/Etats-Unis (2 aut., 4 aut., 5 aut., 6 aut., 7 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Neurology; ISSN 0028-3878; Coden NEURAI; Etats-Unis; Da. 1997; Vol. 48; No. 6; Pp. 1578-1583; Bibl. 21 ref. |
LA : | Anglais |
EA : | Article abstract-To estimate the threshold of nigrostriatal dysfunction required for symptomatic Parkinson's disease (PD), we employed [11C ]RTI-32 and PET to study the dopamine transporter in striatal subdivisions of 11 L-dopa-naive patients with very early parkinsonism. As compared with the controls (N = 10), the PD group had on the side contralateral to the maximal clinical symptoms, significantly reduced binding in the posterior putamen (-56%) and anterior putamen (-28%), with the reduction in caudate (- 12%) not significantly different. To the extent that dopamine transporter binding accurately reflects the number of nigrostriatal dopamine nerve terminals, these findings suggest that the clinical threshold for PD in the middle-age human is approximately 50% loss of dopaminergic innervation to the posterior putamen. Our data also suggest that damage to the putamen component of the striatum is sufficient for the clinical expression of PD. |
CC : | 002B17G |
FD : | Parkinson maladie; Tomoscintigraphie; Positon; Dopamine; Protéine transport; Précoce; Exploration; Homme |
FG : | Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Exploration radioisotopique |
ED : | Parkinson disease; Emission tomography; Positron; Dopamine; Carrier protein; Early; Exploration; Human |
EG : | Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Radionuclide study |
GD : | Positron |
SD : | Parkinson enfermedad; Tomocentelleografía; Positrón; Dopamina; Proteína transportador; Precoz; Exploración; Hombre |
LO : | INIST-6345.354000061850460190 |
ID : | 97-0355687 |
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Pascal:97-0355687Le document en format XML
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<front><div type="abstract" xml:lang="en">Article abstract-To estimate the threshold of nigrostriatal dysfunction required for symptomatic Parkinson's disease (PD), we employed [<sup>11</sup>
C ]RTI-32 and PET to study the dopamine transporter in striatal subdivisions of 11 L-dopa-naive patients with very early parkinsonism. As compared with the controls (N = 10), the PD group had on the side contralateral to the maximal clinical symptoms, significantly reduced binding in the posterior putamen (-56%) and anterior putamen (-28%), with the reduction in caudate (- 12%) not significantly different. To the extent that dopamine transporter binding accurately reflects the number of nigrostriatal dopamine nerve terminals, these findings suggest that the clinical threshold for PD in the middle-age human is approximately 50% loss of dopaminergic innervation to the posterior putamen. Our data also suggest that damage to the putamen component of the striatum is sufficient for the clinical expression of PD.</div>
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<ET>[<sup>11</sup>
C]RTI-32 PET studies of the dopamine transporter in early dopa-naive Parkinson's disease : Implications for the symptomatic threshold</ET>
<AU>GUTTMAN (M.); BURKHOLDER (J.); KISH (S. J.); HUSSEY (D.); WILSON (A.); DASILVA (J.); HOULE (S.)</AU>
<AF>Human Neurochemical Pathology Laboratory/Canada (1 aut., 3 aut.); Clarke Institute of Psychiatry, Division of Neurology, University of Toronto Faculty of Medicine/Toronto, Ontario/Canada (1 aut.); PET Center/Etats-Unis (2 aut., 4 aut., 5 aut., 6 aut., 7 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Neurology; ISSN 0028-3878; Coden NEURAI; Etats-Unis; Da. 1997; Vol. 48; No. 6; Pp. 1578-1583; Bibl. 21 ref.</SO>
<LA>Anglais</LA>
<EA>Article abstract-To estimate the threshold of nigrostriatal dysfunction required for symptomatic Parkinson's disease (PD), we employed [<sup>11</sup>
C ]RTI-32 and PET to study the dopamine transporter in striatal subdivisions of 11 L-dopa-naive patients with very early parkinsonism. As compared with the controls (N = 10), the PD group had on the side contralateral to the maximal clinical symptoms, significantly reduced binding in the posterior putamen (-56%) and anterior putamen (-28%), with the reduction in caudate (- 12%) not significantly different. To the extent that dopamine transporter binding accurately reflects the number of nigrostriatal dopamine nerve terminals, these findings suggest that the clinical threshold for PD in the middle-age human is approximately 50% loss of dopaminergic innervation to the posterior putamen. Our data also suggest that damage to the putamen component of the striatum is sufficient for the clinical expression of PD.</EA>
<CC>002B17G</CC>
<FD>Parkinson maladie; Tomoscintigraphie; Positon; Dopamine; Protéine transport; Précoce; Exploration; Homme</FD>
<FG>Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Exploration radioisotopique</FG>
<ED>Parkinson disease; Emission tomography; Positron; Dopamine; Carrier protein; Early; Exploration; Human</ED>
<EG>Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Radionuclide study</EG>
<GD>Positron</GD>
<SD>Parkinson enfermedad; Tomocentelleografía; Positrón; Dopamina; Proteína transportador; Precoz; Exploración; Hombre</SD>
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