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      Diagnostic Value of 123I-Ioflupane and 123I-Iodobenzamide SPECT Scans in 248 Patients with Parkinsonian Syndromes

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          Abstract

          Background: SPECT is one of the most employed techniques in the diagnostic workup of idiopathic Parkinson’s disease (IPD). Despite its widespread use, the exact diagnostic accuracy of this technique in parkinsonian syndromes remains controversial. Methods: In this study, we investigated the diagnostic accuracy of an initial <sup>123</sup>I-ioflupane (FP-CIT) and/or <sup>123</sup>I-iodobenzamide (IBZM) SPECT to differentiate between IPD and other parkinsonian disorders. 248 patients underwent a SPECT scan because of an as yet unclassified parkinsonian syndrome in our clinic between 2001 and 2006. Gold standard was the clinical diagnosis derived from the latest available clinical record, or, when this was not possible, a new complete physical and neurological examination by a blinded movement disorder specialist neurologist. Mean follow-up between SPECT and the latest clinical information was 18 months (range 3 months to 5 years). Results: 223 of the 248 patients were clinically definitely diagnosed after follow-up: IPD 127, atypical parkinsonian syndromes (APS) 27, essential tremor (ET) 22, vascular parkinsonism (VP) 16, drug-induced parkinsonism (DIP) 5, doubt between PD and APS 2, other diseases without dopaminergic involvement 24. The mean odds ratio (95% CI) for FP-CIT SPECT’s ability to distinguish between IPD and ET was 82 (11–674); between IPD and VP 61 (8–490); between IPD and DIP 36 (2–697) and between IPD and APS was 1 (0–4). The odds ratio for the IBZM SPECT tracer to differentiate between IPD and APS was 7 (2–17). Conclusions: FP-CIT SPECT is accurate to differentiate patients with IPD from those with ET, and IPD from VP and DIP. The accuracy of both FP-CIT and IBZM SPECT scans to differentiate between IPD and APS is low.

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          Most cited references28

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          The accuracy of diagnosis of parkinsonian syndromes in a specialist movement disorder service.

          We have reviewed the clinical and pathological diagnoses of 143 cases of parkinsonism seen by neurologists associated with the movement disorders service at The National Hospital for Neurology and Neurosurgery in London who came to neuropathological examination at the United Kingdom Parkinson's Disease Society Brain Research Centre, over a 10-year period between 1990 and the end of 1999. Seventy-three (47 male, 26 female) cases were diagnosed as having idiopathic Parkinson's disease (IPD) and 70 (42 male, 28 female) as having another parkinsonian syndrome. The positive predictive value of the clinical diagnosis for the whole group was 85.3%, with 122 cases correctly clinically diagnosed. The positive predictive value of the clinical diagnosis of IPD was extremely high, at 98.6% (72 out of 73), while for the other parkinsonian syndromes it was 71.4% (50 out of 70). The positive predictive values of a clinical diagnosis of multiple system atrophy (MSA) and progressive supranuclear palsy (PSP) were 85.7 (30 out of 35) and 80% (16 out of 20), respectively. The sensitivity for IPD was 91.1%, due to seven false-negative cases, with 72 of the 79 pathologically established cases being diagnosed in life. For MSA, the sensitivity was 88.2% (30 out of 34), and for PSP it was 84.2% (16 out of 19). The diagnostic accuracy for IPD, MSA and PSP was higher than most previous prospective clinicopathological series and studies using the retrospective application of clinical diagnostic criteria. The seven false-negative cases of IPD suggest a broader clinical picture of disease than previously thought acceptable. This study implies that neurologists with particular expertise in the field of movement disorders may be using a method of pattern recognition for diagnosis which goes beyond that inherent in any formal set of diagnostic criteria.
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            We report the results of a consensus conference on the diagnosis of multiple system atrophy (MSA). We describe the clinical features of the disease, which include four domains: autonomic failure/urinary dysfunction, parkinsonism and cerebellar ataxia, and corticospinal dysfunction. We set criteria to define the relative importance of these features. The diagnosis of possible MSA requires one criterion plus two features from separate other domains. The diagnosis of probable MSA requires the criterion for autonomic failure/urinary dysfunction plus poorly levodopa responsive parkinsonism or cerebellar ataxia. The diagnosis of definite MSA requires pathological confirmation.
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              Clinicopathological investigation of vascular parkinsonism, including clinical criteria for diagnosis.

              Vascular parkinsonism (VP) is difficult to diagnose with any degree of clinical certainty. We investigated the importance of macroscopic cerebral infarcts and pathological findings associated with microscopic "small vessel disease" (SVD) in the aetiology of VP. The severity of microscopic SVD pathology (perivascular pallor, gliosis, hyaline thickening, and enlargement of perivascular spaces) and the presence of macroscopically visible infarcts were assessed in 17 patients with parkinsonism and no pathological evidence of either Parkinson's disease or any histopathological condition known to be associated with a parkinsonian syndrome, and compared with age-matched controls. Microscopic SVD pathology was significantly more severe in the parkinsonian brains. Most patients presented with bilateral bradykinesia and rigidity together with a gait disorder characterised predominantly by a shuffling gait. Four patients presented acutely with hemiparesis and then progressed to develop a parkinsonian syndrome. They could be distinguished from the remaining VP patients by the presence at autopsy of macroscopically visible lacunar infarcts in regions where contralateral thalamocortical drive might be reduced. The clinical features at presentation varied according to the speed of onset and the underlying vascular pathological state. New clinical criteria for a diagnosis of VP are proposed based on the clinicopathological findings of this study. Copyright 2004 Movement Disorder Society
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                Author and article information

                Journal
                ENE
                Eur Neurol
                10.1159/issn.0014-3022
                European Neurology
                S. Karger AG
                0014-3022
                1421-9913
                2008
                April 2008
                08 February 2008
                : 59
                : 5
                : 258-266
                Affiliations
                Departments of aNeurology, bClinical Epidemiology and Technology Assessment, cClinical Neurophysiology and dNuclear Medicine, University Hospital Maastricht, Maastricht, The Netherlands
                Article
                115640 Eur Neurol 2008;59:258–266
                10.1159/000115640
                18264015
                1c2a50c4-f614-48d4-9266-f5cf3da1acec
                © 2008 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                : 06 June 2007
                : 18 September 2007
                Page count
                Figures: 2, Tables: 3, References: 49, Pages: 9
                Categories
                Original Paper

                Geriatric medicine,Neurology,Cardiovascular Medicine,Neurosciences,Clinical Psychology & Psychiatry,Public health
                123I-ioflupane,Single Photon Emission Computed Tomography,Idiopathic Parkinson’s disease, 123I-iodobenzamide,Parkinsonism

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