Striatal dopamine transporter in dementia with Lewy bodies and Parkinson disease - A comparison

Walker, Zuzana and Costa, Durval and Walker, Rick and Lee, Lean and Livingston, Gill and Jaros, Evelyn and Perry, Robert and McKeith, Ian and Katona, Cornelius (2004) Striatal dopamine transporter in dementia with Lewy bodies and Parkinson disease - A comparison. Neurology, 62 (9). pp. 1568-1572. ISSN 0028-3878. (The full text of this publication is not available from this repository)

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Abstract

Objective: To study the nigrostriatal pathways in 21 patients with dementia with Lewy bodies (DLB), 19 drug naive Parkinson disease (PD) patients, and 16 controls using a dopaminergic presynaptic ligand [I-123]-2beta-carbometoxy-3beta-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (FP-CIT) and SPECT in order to assess similarities or differences between DLB and PD. Methods: A SPECT scan was carried out 3 to 4 hours after administration of 185 MBq (IV) of FP-CIT. Using occipital cortex as a radioactivity uptake reference, ratios for the caudate nuclei and the anterior and posterior putamina of both hemispheres were calculated. From the FP-CIT binding measurements, asymmetry indices and caudate: putamen ratios were derived. Results: The DLB and PD groups had lower FP-CIT binding in all striatal areas than controls (analysis of variance: p < 0.001 in all measures). DLB patients also had significantly lower binding in the caudate nucleus than the PD patients. There was greater asymmetry of uptake in the posterior putamina of PD patients than DLB patients (p < 0.04) and controls (p < 0.01). The mean caudate: putamen ratio for the DLB group was not significantly different from that of the controls, while the mean caudate: putamen ratio of the PD group was higher than that of the control group (p < 0.001) and the DLB group (p < 0.001). Conclusion: This study showed differences between PD and DLB in the pattern of striatal dopaminergic dysfunction. DLB patients do not have the characteristic selective degeneration of ventrolateral nigral neurons seen in PD. This could explain some of the clinical differences between DLB and PD.

Item Type: Article
Additional information: NOT IN FILE
Subjects: R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
Divisions: Faculties > Science Technology and Medical Studies > Kent Institute of Medicine and Health Sciences (KIMHS)
Depositing User: M.P. Stone
Date Deposited: 02 Oct 2008 16:55
Last Modified: 16 Jul 2014 11:22
Resource URI: http://kar.kent.ac.uk/id/eprint/12303 (The current URI for this page, for reference purposes)
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