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194 results on '"Grandas F"'

9. Efficacy and safety of pallidal stimulation in primary dystonia: results of the Spanish multicentric study

Author

Valldeoriola, F., Regidor, I., Minguez-Castellanos, A., Lezcano, E., Garcia-Ruiz, P., Rojo, A., Salvador, A., Castro, A., Grandas, F., Kulisevsky, J., Marti, M.J., Martinez-Martin, P., Relova, L., Rumia, J., Camara, A., Burguera, J.A., Linzasoro, G., Lopez de Val, J., Obeso, J., Rodriguez-Oroz, M.C., and Tolosa, E.

Subjects
Dystonia -- Care and treatment, Dystonia -- Research, Neural stimulation -- Patient outcomes, Neural stimulation -- Research, Health, Psychology and mental health
Published
2010

16. EFNS/MDS-ES recommendations for the diagnosis of Parkinsonʼs disease

Author

Berardelli, A., Wenning, G. K., Antonini, A., Berg, D., Bloem, B. R., Bonifati, V., Brooks, D., Burn, D. J., Colosimo, C., Fanciulli, A., Ferreira, J., Gasser, T., Grandas, F., Kanovsky, P., Kostic, V., Kulisevsky, J., Oertel, W., Poewe, W., Reese, J.-P., Relja, M., Ruzicka, E., Schrag, A., Seppi, K., Taba, P., and Vidailhet, M.

Published
2013
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17. EFNS/MDS-ES recommendations for the diagnosis of Parkinsonʼs disease: FW 4-4

Author

Berardelli, A., Wenning, G., Antonini, A., Berg, D., Bloem, B. R., Bonifati, V., Brooks, D., Burn, David, Colosimo, C., Ferreira, J., Gasser, T., Grandas, F., Kanovsky, P., Kostic, V., Kulisevsky, J., Oertel, W., Poewe, W., Reese, J.-P., Relja, M., Ruzicka, E., Schapira, A., Schrag, A., Seppi, K., Taba, P., and Vidailhet, M.

Published
2012

31. Levodopa in the treatment of Parkinson's disease: Current controversies.

Author

Olanow, C. Warren, Agid, Yves, Mizuno, Yoshi, Albanese, Alberto, Bonucelli, U., Damier, Philip, De Yebenes, Justo, Gershanik, Oscar, Guttman, Mark, Grandas, F., Hallett, Mark, Hornykiewicz, Ole, Jenner, Peter, Katzenschlager, R., Langston, William J., LeWitt, Peter, Melamed, Eldad, Mena, M.A., Michel, P.P., and Mytilineou, Catherine

Abstract

Levodopa is the most effective symptomatic agent in the treatment of Parkinson's disease (PD) and the 'gold standard' against which new agents must be compared. However, there remain two areas of controversy: (1) whether levodopa is toxic, and (2) whether levodopa directly causes motor complications. Levodopa is toxic to cultured dopamine neurons, and this may be a problem in PD where there is evidence of oxidative stress in the nigra. However, there is little firm evidence to suggest that levodopa is toxic in vivo or in PD. Clinical trials have not clarified this situation. Levodopa is also associated with motor complications. Increasing evidence suggests that they are related, at least in part, to the short half-life of the drug (and its potential to induce pulsatile stimulation of dopamine receptors) rather than to specific properties of the molecule. Treatment strategies that provide more continuous stimulation of dopamine receptors provide reduced motor complications in MPTP monkeys and PD patients. These studies raise the possibility that more continuous and physiological delivery of levodopa might reduce the risk of motor complications. Clinical trials to test this hypothesis are underway. We review current evidence relating to these areas of controversy. © 2004 Movement Disorder Society [ABSTRACT FROM AUTHOR]

Published
2004
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36. REVIEW.

Author

Obeso, J. A., Grandas, F., Herrero, M. T., and Horowski, R.

Published
1994
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37. Blepharospasm: a review of 264 patients.

Author

Grandas, F, Elston, J, Quinn, N, and Marsden, C D

Abstract

The natural history and response to different treatments have been evaluated in 264 patients with blepharospasm. The mean age of onset was 55.8 years and there was a female preponderance of 1.8 to 1. Dystonia elsewhere was found in 78% of patients, usually in the cranial-cervical region, and appeared to follow a somatotopic progression. A family history of blepharospasm or dystonia elsewhere was found in 9.5% of cases, which suggests a genetic predisposition. Ocular lesions preceded the onset of blepharospasm in 12.1% of cases. The response to drugs was inconsistent, although initial improvement was experienced by one fifth of patients treated with anticholinergics. Twenty-nine bilateral facial nerve avulsion operations were performed with benefit in 27 cases; but recurrences appeared in 22, on average one year after surgery. Botulinum toxin injections were performed in 151 patients. Significant improvement was achieved in 118 cases. Mean duration of benefit was 9.2 weeks. Transient ptosis and diplopia were the commonest side effects. [ABSTRACT FROM AUTHOR]

Published
1988
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40. Letters to the editor.

Author

Grandas, F., Quinn, N., Elston, J., Marsden, C. D., Walters, Arthur S., Hening, Wayne, Chokroverty, Sudhansu, Imai, Hisamasa, Narabayashi, Hirotaro, Quinn, Niall, and Marsden, C. David

Published
1990
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50. Relevance of genetic testing in the gene-targeted trial era: the Rostock Parkinson's disease study.

Author

Westenberger A, Skrahina V, Usnich T, Beetz C, Vollstedt EJ, Laabs BH, Paul JJ, Curado F, Skobalj S, Gaber H, Olmedillas M, Bogdanovic X, Ameziane N, Schell N, Aasly JO, Afshari M, Agarwal P, Aldred J, Alonso-Frech F, Anderson R, Araújo R, Arkadir D, Avenali M, Balal M, Benizri S, Bette S, Bhatia P, Bonello M, Braga-Neto P, Brauneis S, Cardoso FEC, Cavallieri F, Classen J, Cohen L, Coletta D, Crosiers D, Cullufi P, Dashtipour K, Demirkiran M, de Carvalho Aguiar P, De Rosa A, Djaldetti R, Dogu O, Dos Santos Ghilardi MG, Eggers C, Elibol B, Ellenbogen A, Ertan S, Fabiani G, Falkenburger BH, Farrow S, Fay-Karmon T, Ferencz GJ, Fonoff ET, Fragoso YD, Genç G, Gorospe A, Grandas F, Gruber D, Gudesblatt M, Gurevich T, Hagenah J, Hanagasi HA, Hassin-Baer S, Hauser RA, Hernández-Vara J, Herting B, Hinson VK, Hogg E, Hu MT, Hummelgen E, Hussey K, Infante J, Isaacson SH, Jauma S, Koleva-Alazeh N, Kuhlenbäumer G, Kühn A, Litvan I, López-Manzanares L, Luxmore M, Manandhar S, Marcaud V, Markopoulou K, Marras C, McKenzie M, Matarazzo M, Merello M, Mollenhauer B, Morgan JC, Mullin S, Musacchio T, Myers B, Negrotti A, Nieves A, Nitsan Z, Oskooilar N, Öztop-Çakmak Ö, Pal G, Pavese N, Percesepe A, Piccoli T, Pinto de Souza C, Prell T, Pulera M, Raw J, Reetz K, Reiner J, Rosenberg D, Ruiz-Lopez M, Ruiz Martinez J, Sammler E, Santos-Lobato BL, Saunders-Pullman R, Schlesinger I, Schofield CM, Schumacher-Schuh AF, Scott B, Sesar Á, Shafer SJ, Sheridan R, Silverdale M, Sophia R, Spitz M, Stathis P, Stocchi F, Tagliati M, Tai YF, Terwecoren A, Thonke S, Tönges L, Toschi G, Tumas V, Urban PP, Vacca L, Vandenberghe W, Valente EM, Valzania F, Vela-Desojo L, Weill C, Weise D, Wojcieszek J, Wolz M, Yahalom G, Yalcin-Cakmakli G, Zittel S, Zlotnik Y, Kandaswamy KK, Balck A, Hanssen H, Borsche M, Lange LM, Csoti I, Lohmann K, Kasten M, Brüggemann N, Rolfs A, Klein C, and Bauer P

Subjects
Humans, Male, Female, Middle Aged, Aged, Glucosylceramidase genetics, alpha-Synuclein genetics, Genetic Predisposition to Disease, Ubiquitin-Protein Ligases genetics, Cohort Studies, Protein Kinases genetics, Mutation, Adult, Parkinson Disease genetics, Genetic Testing methods, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 genetics
Abstract

Estimates of the spectrum and frequency of pathogenic variants in Parkinson's disease (PD) in different populations are currently limited and biased. Furthermore, although therapeutic modification of several genetic targets has reached the clinical trial stage, a major obstacle in conducting these trials is that PD patients are largely unaware of their genetic status and, therefore, cannot be recruited. Expanding the number of investigated PD-related genes and including genes related to disorders with overlapping clinical features in large, well-phenotyped PD patient groups is a prerequisite for capturing the full variant spectrum underlying PD and for stratifying and prioritizing patients for gene-targeted clinical trials. The Rostock Parkinson's disease (ROPAD) study is an observational clinical study aiming to determine the frequency and spectrum of genetic variants contributing to PD in a large international cohort. We investigated variants in 50 genes with either an established relevance for PD or possible phenotypic overlap in a group of 12 580 PD patients from 16 countries [62.3% male; 92.0% White; 27.0% positive family history (FH+), median age at onset (AAO) 59 years] using a next-generation sequencing panel. Altogether, in 1864 (14.8%) ROPAD participants (58.1% male; 91.0% White, 35.5% FH+, median AAO 55 years), a PD-relevant genetic test (PDGT) was positive based on GBA1 risk variants (10.4%) or pathogenic/likely pathogenic variants in LRRK2 (2.9%), PRKN (0.9%), SNCA (0.2%) or PINK1 (0.1%) or a combination of two genetic findings in two genes (∼0.2%). Of note, the adjusted positive PDGT fraction, i.e. the fraction of positive PDGTs per country weighted by the fraction of the population of the world that they represent, was 14.5%. Positive PDGTs were identified in 19.9% of patients with an AAO ≤ 50 years, in 19.5% of patients with FH+ and in 26.9% with an AAO ≤ 50 years and FH+. In comparison to the idiopathic PD group (6846 patients with benign variants), the positive PDGT group had a significantly lower AAO (4 years, P = 9 × 10-34). The probability of a positive PDGT decreased by 3% with every additional AAO year (P = 1 × 10-35). Female patients were 22% more likely to have a positive PDGT (P = 3 × 10-4), and for individuals with FH+ this likelihood was 55% higher (P = 1 × 10-14). About 0.8% of the ROPAD participants had positive genetic testing findings in parkinsonism-, dystonia/dyskinesia- or dementia-related genes. In the emerging era of gene-targeted PD clinical trials, our finding that ∼15% of patients harbour potentially actionable genetic variants offers an important prospect to affected individuals and their families and underlines the need for genetic testing in PD patients. Thus, the insights from the ROPAD study allow for data-driven, differential genetic counselling across the spectrum of different AAOs and family histories and promote a possible policy change in the application of genetic testing as a routine part of patient evaluation and care in PD., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Guarantors of Brain.)

Published
2024
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