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Two interesting reports from the just concluded PD conference in Helsinki. --------- Forwarded message ---------- From: WE MOVE <[log in to unmask]> To: <[log in to unmask]> Date: Fri, 3 Aug 2001 13:35:07 -0500 Subject: No Acceleration of Dyskinesias After Ropinirole Monotherapy (PD Congress 2001) Message-ID: <[log in to unmask]> E-MOVE reports from the 14th International Congress on Parkinson's Disease, Helsinki July 28-Aug 1. Poster and Platform session numbers refer to those in the abstract book, published in Parkinsonism and Related Disorders 2001;7(Supplement). The development of dyskinesia in Parkinson's disease patients receiving ropinirole and given supplementary levodopa O Rascol, DJ Brooks, CE Clarke, PP DeDeyn, AD Korczyn, AE Lang, M Abdallah P-TU-226 The rate of dyskinesia development does not increase when levodopa is added to monotherapy with ropinirole, according to this report. This study addressed the question of whether the proven dyskinesia-delaying effect of early monotherapy with a dopamine agonist would be lost when addition of levodopa was required for symptom control in later PD. Patients in this study were a subset of the 056 study of ropinirole as monotherapy (see http://www.wemove.org/ema/em_pd_01.html). Time to development of dyskinesias for patients randomized to initial levodopa treatment (n=89) was compared to time for ropinirole patients following their initiation of supplemental levodopa (n=179). No significant difference between the groups was found. A series of analyses was applied to determine if results were affected by any of several confounding factors, including age, disease state, and total daily levodopa dose at dyskinesia onset. No effect was found for any of these factors. The authors conclude that these results indicate "ropinirole delayed the development of dyskinesia by delaying the onset of levodopa therapy," and that the data argue against major effects on dyskinesia development in this population from either a positive protective effect of ropinirole, or simple disease duration. Supported by Glaxo SmithKline ----------------------------------------------------------- From: WE MOVE <[log in to unmask]> To: <[log in to unmask]> Date: Fri, 3 Aug 2001 11:35:40 -0500 Subject: Ultrasound Abnormalities in the Substantia Nigra (PD Congress 2001) E-MOVE reports from the 14th International Congress on Parkinson's Disease, Helsinki July 28-Aug 1. Poster and Platform session numbers refer to those in the abstract book, published in Parkinsonism and Related Disorders 2001;7(Supplement). 1. Transcranial sonography of the substantia nigra (SN) in patients with idiopathic Parkinson syndrome (IPS), atypical Parkinson syndrome, and controls U Sommer, G Gahn, G Becker, H Reichmann P-MO-037 Parkinson's disease patients have an increased echogenicity of the substantia nigra that can be detected by noninvasive transcranial ultrasound, according to this report. In this technique, ultrasonography is performed through the preauricular acoustic bone window. Twelve PD patients (ages 40-70), 3 atypical parkinsonism patients (2 MSA, 1 PSP), and 12 controls, underwent ultrasound imaging of the substantia nigra. In controls, mean hyperechogenic area was 8.2 square mm (range 4.1-11.1), while in PD patients mean area was 33.2 square mm (range 21.6-62.8), significant at p<0.001. Atypical parkinsonism patients had a mean area of 18.1 square mm (range 16.3-20.6), significantly different from both controls (p<0.001) and PD patients (p<0.05). The authors conclude, "These results confirm...that a hyperechogenic signal alteration in the SN is highly sensitive for idiopathic Parkinson's disease," and suggest that, in light of other results below, ultrasound of the SN may provide a noninvasive technique for identifying persons at risk for developing PD. 2. Susceptibility marker for Parkinson's disease detected by transcranial ultrasound D Berg, G Becker P-MO-027 Ultrasound hyperechogenicity of the substantia nigra correlates with reduced 18F-dopa uptake and increased SN iron deposition in non-PD subjects, according to this report. In this study, 20 healthy subjects below age 40 with SN hyperechogenicity underwent PET imaging. 18F-dopa uptake was reduced compared to controls without SN hyperechogenicity (p<0.05), despite normal neuropsychological and motor performance. In a separate experiment, post-mortem ultrasound and biochemical analysis of 20 patients who died without extrapyramidal disorders showed a correlation between hyperechogenicity and increased iron content in the substantia nigra. The authors suggest this technique provides a useful non-invasive tool for identification of reduced dopaminergic innervation in the substantia nigra. 2. Echogenicity of substantia nigra determined by transcranial ultrasound correlates with severity of parkinsonian symptoms induced by neuroleptic therapy D Berg, B Jabs, U Merschdorf, H Beckmann, G Becker P-WE-463 Patients at risk for neuroleptic-induced parkinsonism have increased ultrasound echogenicity in the substantia nigra, according to this report. Fifty-two psychiatric patients with severe neuroleptic-induced parkinsonism showed significantly increased signal from the SN compared to 41 patients with little or no parkinsonism (p<0.01). Eleven patients requiring neuroleptic treatment underwent transcranial ultrasonography before treatment. Evaluation of parkinsonian symptoms following treatment revealed more severe symptoms in patients who had SN hyperechogenicity (p<0.01). --- Funding for E-MOVE meeting reports is provided in part by unrestricted educational grants from Allergan Inc., Elan Pharmaceuticals, and Pharmacia Corporation. Copyright 2000 WE MOVE Editor: Richard Robinson ([log in to unmask]) This service is provided free of charge to the Internet community, courtesy of WEMOVE.org. This document may be freely redistributed by email only in its unedited form. We encourage you to share it with your colleagues. E-MOVE archives, plus information on subscribing, are available at http://www.wemove.org/emove. To unsubscribe, send an e-mail to [log in to unmask], with "unsubscribe e-move" in the message body. 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